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Biomedical subjects

C R Lo

Publications and source records attributed to C R Lo.

12 recordsLinked to original sources
PubMed2002

Unusual thickness-dependent heat-capacity anomalies in free-standing hexatic liquid-crystal films.

High-resolution heat-capacity and optical-reflectivity measurements have been conducted near the smectic-A to hexatic-B transition in thin free-standing films of the liquid-crystal compound 64COOBC. We find an unexpected dependence on film thickness of the integrated magnitude of the heat-capacity anomalies as the films undergo layer-by-layer transitions. We measure the penetration depths of the ordering from the surface and next-to-surface layers which are pertinent to the highly correlated thermal behavior.

Journal Article↗
PubMed2001

Unusual thickness-dependent thermal behavior and anticlinic coupling in chiral smectic free-standing liquid-crystal films.

We observe, in free-standing films of a chiral smectic liquid crystal, a series of discrete transitions in the relative orientation of the tilt of the interior and surface layers. These transitions include a remarkable reentrant synclinic-anticlinic-synclinic ordering sequence of the film surfaces in the presence of an electric field upon cooling. The profiles of the associated heat-capacity anomalies are found to be strongly thickness dependent and exhibit a novel crossover behavior in reduced dimensions. We measure the anticlinic coupling between tilted surface layers in the smectic- A phase.

Journal Article↗
PubMed2000

Inhibition of c-Myc expression sensitizes hepatocytes to tumor necrosis factor-induced apoptosis and necrosis.

The typical proliferative response of hepatocytes to tumor necrosis factor (TNF) can be converted to a cytotoxic one by transcriptional arrest. Although NF-kappaB activation is critical for hepatocyte resistance to TNF toxicity, the contribution of other TNF-inducible transcription factors remains unknown. To determine the function of c-Myc in hepatocyte sensitivity to TNF, stable transfectants of the rat hepatocyte cell line RALA255-10G containing sense and antisense c-myc expression vectors were isolated with increased (S-Myc cells) and decreased (AN-Myc cells) c-Myc transcriptional activity. While S-Myc cells proliferated in response to TNF treatment, AN-Myc cells underwent 32% cell death within 6 h. Fluorescent microscopic studies indicated that TNF induced apoptosis and necrosis in AN-Myc cells. Cell death was associated with DNA hypoploidy and poly(ADP-ribose) polymerase cleavage but occurred in the absence of detectable caspase-3, -7, or -8 activation. TNF-induced, AN-Myc cell death was dependent on Fas-associated protein with death domain and partially blocked by caspase inhibitors. AN-Myc cells had decreased levels of NF-kappaB transcriptional activity, but S-Myc cells maintained resistance to TNF despite NF-kappaB inactivation, suggesting that c-Myc and NF-kappaB independently mediate TNF resistance. Thus, in the absence of sufficient c-Myc expression, hepatocytes are sensitized to TNF-induced apoptosis and necrosis. These findings demonstrate that hepatocyte resistance to TNF is regulated by multiple transcriptional activators.

Animals↗
PubMed2000

Hepatocytes sensitized to tumor necrosis factor-alpha cytotoxicity undergo apoptosis through caspase-dependent and caspase-independent pathways.

Hepatocytes can be sensitized to tumor necrosis factor (TNF)-alpha toxicity by repression of NF-kappaB activation or inhibition of RNA synthesis. To determine whether both forms of sensitization lead to TNF-alpha cytotoxicity by similar mechanisms, TNF-alpha-induced cell death in RALA255-10G hepatocytes was examined following infection with an adenovirus, Ad5IkappaB, that blocks NF-kappaB activation or following cotreatment with actinomycin D (ActD). TNF-alpha treatment of Ad5IkappaB-infected cells resulted in 44% cell death within 6 h. ActD/TNF-alpha induced no death within 6 h but did lead to 37% cell death by 24 h. In both instances, cell death occurred by apoptosis and was associated with caspase activation, although caspase activation in ActD-sensitized cells was delayed. CrmA and chemical caspase inhibitors blocked Ad5IkappaB/TNF-alpha-induced cell death but did not inhibit ActD/TNF-alpha-induced apoptosis. A Fas-associated protein with death domain (FADD) dominant negative decreased Ad5IkappaB/TNF-alpha- and ActD/TNF-alpha-induced cell death by 81 and 47%, respectively. However, downstream events differed, since Ad5IkappaB/TNF-alpha but not ActD/TNF-alpha treatment caused mitochondrial cytochrome c release. These results suggest that NF-kappaB inactivation and inhibition of RNA synthesis sensitize RALA255-10G hepatocytes to TNF-alpha toxicity through distinct cell death pathways that diverge below the level of FADD. ActD-induced hepatocyte sensitization to TNF-alpha cytotoxicity occurs through a FADD-dependent, caspase-independent pathway of apoptosis.

Adaptor Proteins, Signal Transducing↗
PubMed2000

Role of caspases and NF-kappaB signaling in hydrogen peroxide- and superoxide-induced hepatocyte apoptosis.

Reactive oxygen intermediates (ROI) have been implicated as mediators of hepatocyte death resulting from a variety of forms of liver injury. To delineate the mechanisms that underlie ROI-induced apoptosis, the roles of caspase activation and nuclear factor-kappaB (NF-kappaB) signaling were determined in the rat hepatocyte cell line RALA255-10G after treatment with H(2)O(2) or the superoxide generator menadione. By 8 h, H(2)O(2) and menadione caused 26% and 33% cell death, respectively. Death from both ROI occurred by apoptosis as indicated by morphology under fluorescence microscopy, the induction of caspase activation and DNA fragmentation, and the cleavage of poly(ADP-ribose) polymerase. Despite the presence of caspase activation in both forms of apoptosis, caspase inhibition blocked H(2)O(2)- but not menadione-induced apoptosis. In contrast, inhibition of NF-kappaB activation decreased cell death from both ROI. Different ROI, therefore, induce distinct apoptotic pathways in RALA hepatocytes that are both caspase dependent and independent. In contrast to the known protective effect of NF-kappaB activation in tumor necrosis factor-alpha-induced hepatocyte apoptosis, NF-kappaB promotes hepatocellular death from ROI in these cells.

Animals↗
PubMed1999

Ceramide induces caspase-independent apoptosis in rat hepatocytes sensitized by inhibition of RNA synthesis.

Ceramide has been implicated as a second messenger in intracellular signaling pathways leading to apoptosis in nonhepatic cells. To determine whether ceramide can mediate hepatocyte apoptosis, the cytotoxicity of ceramide was determined in rat hepatocytes. The rat hepatocyte cell line, RALA255-10G, and primary rat hepatocytes were completely resistant to toxicity from 10 to 100 micromol/L C2 ceramide. Resistance was not the result of a failure to take up ceramide, because ceramide treatment did cause nuclear factor-kappaB (NF-kappaB) activation. Because ceramide may mediate cell death from tumor necrosis factor alpha (TNF-alpha), the ability of RNA synthesis inhibition and NF-kappaB inactivation to sensitize hepatocytes to ceramide toxicity was examined. RALA hepatocytes were sensitized to ceramide toxicity by coadministration of actinomycin D (ActD). Cell death occurred by apoptosis as determined by the presence of morphological evidence of apoptosis, caspase activation, poly(ADP-ribose) polymerase (PARP) degradation, and DNA hypoploidy. Despite the induction of apoptosis associated with caspase activation, cell death from ActD/ceramide was not blocked by caspase inhibition. Inhibition of NF-kappaB activation also sensitized RALA hepatocytes to ceramide toxicity, but to a lesser extent than for TNF-alpha. Thus, unlike many nonhepatic cell types, rat hepatocytes are resistant to cell death from ceramide because of the transcriptionally dependent up-regulation of a protective gene(s). The ability of ActD and NF-kappaB inactivation to sensitize RALA hepatocytes to ceramide toxicity suggests that ceramide may act as a downstream mediator of TNF-alpha toxicity.

Animals↗
PubMed1999

Endometrial wave direction switch and the outcome of in vitro fertilization.

OBJECTIVE: To describe endometrial wavelike activity, endometrial thickness and texture in IVF cycles, and to relate them to IVF outcome. To evaluate wave patterns on the day of hCG administration as a predictor of IVF outcome. DESIGN: Ultrasound study. SETTING: University hospital-based infertility clinic. PATIENT(S): Twenty-eight women undergoing IVF. INTERVENTION(S): Ultrasound examinations were performed at five fixed moments (start ovarian stimulation, hCG administration, ovum pickup (OPU), ET, and 7 days after hCG administration) and at three variable moments in the stimulation period in the cycle. The OPU was performed 2 days after hCG administration; ET was performed 2 or 3 days after that. MAIN OUTCOME MEASURE(S): Endometrial wave pattern, thickness, texture, IVF outcome. RESULT(S): Embryo transfer was performed in 22 cycles. In 73% of the cycles a wave direction switch (WDS) from fundus to cervix (FC) to cervix to fundus (CF) occurred before OPU. Eleven (50%) patients became pregnant. Significantly more FC waves persisted until hCG administration in the cycles in which the patients conceived. Endometrial thickness and texture were unrelated to IVF outcome. CONCLUSION(S): Endometrial wave pattern is associated with pregnancy in IVF. The persisting presence of FC waves until hCG administration (a late WDS) predicts a favorable IVF outcome.

Adult↗
PubMed1996

Endometrial wavelike movements during the menstrual cycle.

OBJECTIVE: To qualify and quantify endometrial waves in regularly cycling women. DESIGN: A prospective transvaginal ultrasound study was performed throughout 23 cycles of 16 healthy women. Wave type and wave frequency were evaluated. SETTING: Normal human volunteers in an academic research environment. PATIENTS: Sixteen healthy regularly cycling women. RESULTS: Of 23 cycles, 19 proved to be ovulatory. Five types of endometrial waves could be distinguished. Waves from cervix to fundus and opposing waves were seen predominantly periovulatorily. Waves from fundus to cervix were absent in the postovulatory phase. Endometrial wavelike activity was most pronounced in the periovulatory phase. CONCLUSIONS: Standardized qualification and quantification of endometrial waves, as described in this study, might shed new light on the underlying mechanisms in selected cases of hitherto unexplained subfertility.

Adult↗
PubMed1982

Self-control of interbeat interval and pulse transit time at rest and during exercise. A preliminary report.

Attempts were made to establish self-control of interbeat interval (IBI) and pulse transit time (PTT) by providing appropriate biofeedback information to volunteers at rest and during dynamic and isometric exercise. Product feedback (IBI X PTT) was found more reliable than simple heart rate (HR) and systolic blood pressure (SBP) during dynamic exercise. It also produced greater increases in IBI and PTT than did habituation or relaxation under the same conditions. Product feedback was also superior to the use of other techniques at rest, but PTT feedback did not produce significant control of pressor responses during isometric exercise. Possible reasons for this failure are discussed. Preliminary results of feedback training given to 7 anginal patients suggest that such procedures might help to lower nitroglycerin consumption, decrease the frequency of anginal attacks and increase exercise tolerance.

Angina Pectoris↗
PubMedDate not supplied

The self-control of the cardiovascular response to exercise using feedback of the product of interbeat interval and pulse transit time.

Feedback of the product of interbeat interval and pulse transit time (this product being a close correlate of the product of heart rate and systolic blood pressure) was compared with relaxation training and simple habituation to the experimental task. The subjects were 36 healthy volunteers tested both when inactive and when cycling on a bicycle ergometer. Subjects receiving product feedback were markedly more successful in minimizing the decrease in interbeat interval and pulse transit time caused by exercise (i.e., their rate pressure product rose less). Subjects who received relaxation training or simply exercised showed similar changes in interbeat interval and pulse transit time. In the inactive subject, the superiority of product feedback was much less evident but it did enable subjects to increase pulse transit time (i.e., decrease systolic blood pressure) compared to the other two conditions, which again did not differ. It is proposed that the superiority of product feedback may relate to its value as an index of sympathetic input to the heart and that such feedback may find clinical application in the treatment of angina pectoris.

Adolescent↗