Three-dimensional measurement of radiographic bone-implant contact lengths of zygomatic implants in zygomatic bone: a retrospective study of 66 implants in 28 patients.

Zygomatic implant treatment is widely applied for severe maxillary atrophy to help rehabilitate the maxillary dentition. This retrospective study was performed to evaluate the actual radiographic bone-implant contact (rBIC) lengths of zygomatic implants. The records of 28 patients who underwent zygomatic implant surgery and subsequent follow-up examinations between August 2013 and September 2018 in the Department of Oral and Maxillofacial Surgery, Taipei Tzu Chi Hospital were reviewed. The surgeries were performed by a single surgeon using the same treatment protocol. All patients had a computed tomography scan at 1year after the surgery. Using three-dimensional imaging software, an investigator measured the rBIC lengths of 66 implants and documented their clinical status. The implant survival rate was 100%. The mean rBIC length was significantly longer in male patients than in female patients (20.80±5.88mm versus 17.79±6.34mm; P=0.028). The mean rBIC length of double zygomatic implants was significantly longer when compared to that of single implants (21.11±6.23mm versus 17.75±5.85mm; P=0.027). This article is novel in reporting the exact rBIC lengths of zygomatic implants in a clinical setting. The results showed that zygomatic implants are a viable treatment modality for full-mouth rehabilitation.

Dominant effect of relative tropical Atlantic warming on major hurricane occurrence.

Here we explore factors potentially linked to the enhanced major hurricane activity in the Atlantic Ocean during 2017. Using a suite of high-resolution model experiments, we show that the increase in 2017 major hurricanes was not primarily caused by La Niña conditions in the Pacific Ocean but rather triggered mainly by pronounced warm sea surface conditions in the tropical North Atlantic. Further, we superimpose a similar pattern of North Atlantic surface warming on data for long-term increasing sea surface temperature (a product of increases in greenhouse gas concentrations and decreases in aerosols) to show that this warming trend will likely lead to even higher numbers of major hurricanes in the future. The key factor controlling Atlantic major hurricane activity appears to be the degree to which the tropical Atlantic warms relative to the rest of the global ocean.

The application of individual virtual nostalgic game design to the evaluation of cognitive function.

The aim of this study was to develop a task set based on personalized material for nostalgic experience, which could detect cognitive ability via a virtual experience system combined with Kinect somatosensory interactive operation applications without the user wearing any accessory input device. Fifty-nine subjects participated in the experiment. The receiver operating characteristic curve of the game system was statistically analyzed for determining the best cutoff-point in the cognitive function assessment. Correlation analysis and regression analysis were used to explore the correlations between the results and the clinical cognitive assessment scales. According to the MoCA scores, the results showed that the accuracy of the system was 86.4% in evaluating mild cognitive impairment. The system seems feasible and was strongly correlated with clinical cognitive assessment scales. We anticipate that daily use of our system could keep track of changes of cognitive function of the elderly in home life.

Purulent pericarditis, multi-site abscesses and ketoacidosis in a patient with newly diagnosed diabetes: a rare case report.

BACKGROUND: Purulent pericarditis is an acute and fulminant disease characterized by pus accumulation in the pericardial space. Its incidence has declined substantially and the common pathogen has changed since the beginning of the antibiotic era; however, it is still found in some patients with immunocompromised conditions. CASE REPORT: We report a rare case in which the onset of diabetes mellitus presented as extremely high HbA1c concentration, ketoacidosis, multi-site abscesses and purulent pericarditis. After antibiotic therapy and pericardiocentesis, the purulent pericarditis still did not resolve and further intrapericardial thrombolytic therapy also failed. Finally, this patient was treated successfully by surgical debridement and pericardiectomy. CONCLUSION: In the immunocompromised state of severe hyperglycaemia, purulent pericarditis is a possible complication of uncontrolled infection. If purulent pericarditis cannot be cured using non-surgical treatments, such as antibiotic therapy, pericardiocentesis and intrapericardial thrombolytic therapy, a surgical pericardiectomy should be considered to avoid morbidity and mortality.

WWOX suppresses autophagy for inducing apoptosis in methotrexate-treated human squamous cell carcinoma.

Squamous cell carcinoma (SCC) cells refractory to initial chemotherapy frequently develop disease relapse and distant metastasis. We show here that tumor suppressor WW domain-containing oxidoreductase (WWOX) (also named FOR or WOX1) regulates the susceptibility of SCC to methotrexate (MTX) in vitro and cure of SCC in MTX therapy. MTX increased WWOX expression, accompanied by caspase activation and apoptosis, in MTX-sensitive SCC cell lines and tumor biopsies. Suppression by a dominant-negative or small interfering RNA targeting WWOX blocked MTX-mediated cell death in sensitive SCC-15 cells that highly expressed WWOX. In stark contrast, SCC-9 cells expressed minimum amount of WWOX protein and resisted MTX-induced apoptosis. Transiently overexpressed WWOX sensitized SCC-9 cells to apoptosis by MTX. MTX significantly downregulated autophagy-related Beclin-1, Atg12-Atg5 and LC3-II protein expression and autophagosome formation in the sensitive SCC-15, whereas autophagy remained robust in the resistant SCC-9. Mechanistically, WWOX physically interacted with mammalian target of rapamycin (mTOR), which potentiated MTX-increased phosphorylation of mTOR and its downstream substrate p70 S6 kinase, along with dramatic downregulation of the aforementioned proteins in autophagy, in SCC-15. When WWOX was knocked down in SCC-15, MTX-induced mTOR signaling and autophagy inhibition were blocked. Thus, WWOX renders SCC cells susceptible to MTX-induced apoptosis by dampening autophagy, and the failure in inducing WWOX expression leads to chemotherapeutic drug resistance.

Antizyme, a natural ornithine decarboxylase inhibitor, induces apoptosis of haematopoietic cells through mitochondrial membrane depolarization and caspases' cascade.

Antizymes delicately regulate ornithine decarboxylase (ODC) enzyme activity and polyamine transportation. One member of the family, antizyme-1, plays vital roles in molecular and cellular functions, including developmental regulation, cell cycle, proliferation, cell death, differentiation and tumorigenesis. However, the question of how does it participate in the cell apoptotic mechanism is still unsolved. To elucidate the contribution of human antizyme-1 in haematopoietic cell death, we examine whether inducible overexpression of antizyme enhances apoptotic cell death. Antizyme reduced the viability in a dose- and time-dependent manner of human leukemia HL-60 cells, acute T leukemia Jurkat cells and mouse macrophage RAW 264.7 cells. The apoptosis-inducing activities were determined by nuclear condensation, DNA fragmentation, sub-G(1) appearance, loss of mitochondrial membrane potential (Deltapsi( m )), release of mitochondrial cytochrome c into cytoplasm and proteolytic activation of caspase 9 and 3. Following conditional antizyme overexpression, all protein levels of cyclin-dependent kinases (Cdks) and cyclins are not significantly reduced, except cyclin D, before their entrance into apoptotic cell death. However, introduced cyclin D1 into Jurkat T tetracycline (Tet)-On cell system still couldn't rescue cells from apoptosis. Antizyme doesn't influence the expression of tumor suppressor p53 and its downstream p21, but it interferes in the expressions of Bcl-2 family. Inducible antizyme largely enters mitochondria resulting in cytochrome c release from mitochondria to cytosol following Bcl-xL decrease and Bax increase. According to these data, we suggest that antizyme induces apoptosis mainly through mitochondria-mediated and cell cycle-independent pathway. Furthermore, antizyme induces apoptosis not only by Bax accumulation reducing the function of the Bcl-2 family, destroying the Deltapsi( m ), and releasing cytochrome c to cytoplasm but also by the activation of apoptosomal caspase cascade.

Increasing ornithine decarboxylase activity is another way of prolactin preventing methotrexate-induced apoptosis: crosstalk between ODC and BCL-2.

Prolactin has more than 300 separate functions including affecting mammary growth, differentiation, secretion and anti-apoptosis. In the previous studies, prolactin induced Bcl-2 expression to prevent apoptosis and also provoked the activity of ornithine decarboxylase (ODC). Our previous data showed that ODC overexpression upregulates Bcl-2 and prevents tumor necrosis factor alpha (TNF-alpha)- and methotrexate (MTX)-induced apoptosis. Here, we further investigate whether prolactin prevents MTX-induced apoptosis through inducing ODC activity and the relationship between ODC and Bcl-2 upon prolactin stimulation. Prolactin prevented MTX-induced apoptosis in a dose-dependent manner in HL-60 cells. Following prolactin stimulation, ODC enzyme activity also shows an increase in a dose-dependent manner, expressing its maximum level at 3 h, and rapidly declining thereafter. Prolactin-induced ODC activity is completely blocked by a protein kinase C delta (PKCdelta) inhibitor, rottlerin. However, there are no changes in the expressions of ODC mRNA and protein level after prolactin stimulus. It indicates that prolactin may induce ODC activity through the PCKdelta pathway. Besides, Bcl-2 expresses within 1 h of prolactin treatment and this initiating effect of prolactin is not inhibited by alpha-difluoromethylornithine (DFMO). However, Bcl-2 is further enhanced following prolactin stimulation for 4 h and this enhancement is blocked by DFMO. Bcl-2 has no effect on ODC activity and protein levels, but ODC upregulates Bcl-2, which is inhibited by DFMO. Overall, there are two different forms of prolactin effect, it induces Bcl-2 primarily, and following this it stimulates ODC activity. Consequently induced ODC activity further enhances the expression of Bcl-2. The anti-apoptotic effect of prolactin is diminished by DFMO and recovered by putrescine. Obviously, ODC activity is one basis for the anti-apoptotic mechanisms of prolactin. A Bcl-2 inhibitor, HA14-1, together with DFMO, completely blocks the anti-apoptotic effects of prolactin. These results suggest that increasing ODC activity is another way of prolactin preventing MTX-induced apoptosis and that this induction of ODC activity enhances the expression of Bcl-2 strongly enough to bring about the anti-apoptotic function.

Overexpression of peptidylarginine deiminase IV features in apoptosis of haematopoietic cells.

Peptidylarginine deiminases (PADIs) convert peptidylarginine into citrulline via posttranslational modification. One member of the family, PADI4, plays an important role in immune cell differentiation and cell death. To elucidate the participation of PADI4 in haematopoietic cell death, we examine whether inducible overexpression of PADI4 enhances the apoptotic cell death. PADI4 reduced the viability in a dose- and time-dependent manner of human leukemia HL-60 cells and human acute T leukemia Jurkat cells. The apoptosis-inducing activities were determined by nuclear condensation, DNA fragmentation, sub-G1 appearance, loss of mitochondrial membrane potential (delta psi(m)), release of mitochondrial cytochrome c into cytoplasm and proteolytic activation of caspase 9 and 3. Following PADI4 overexpression, cells arrest in G1 phase significantly before their entrance into apoptotic cell death. PADI4 increases tumor suppressor p53 and its downstream p21 to control cell cycle. In the detections of protein expression and kinase activity, all protein levels of cyclin-dependent kinases (CDKs) and cyclins are not reduced except cyclin D, however, CDK2 (G1 entry S phase) and CDK1 (G2 entry M phase) enzyme activities are inhibited by conditionally inducible PADI4. p53 also expands its other downstream Bax to induce cytochrome c release from mitochondria. According to these data, we suggest that PADI4 induces apoptosis mainly through cell cycle arrest and mitochondria-mediated pathway. Furthermore, p53 features in PADI4-induced apoptosis by increasing intracellular p21 to control cell cycle and by Bax accumulation to decline Bcl-2 function, destroy delta psi(m), release cytochrome c to cytoplasm and activate the caspase cascade.

Influences of pH and hydraulic retention time on anaerobes converting beer processing wastes into hydrogen.

To convert high-solids organic wastes (3% w./w.) to high-value hydrogen, a full factorial experimental design was employed in planning the experiments for learning the effects of pH and hydraulic retention time (HRT) on the hydrogen production in a chemostat reactor using waste yeast obtained from beer processing wastes. For determining which experimental variable settings affect hydrogen production, predictive polynomial quadratic equation and response surface methodology were employed to determine and explain the conditions required for high-value hydrogen production. Experimental results indicate that a maximum hydrogen production rate of 460 mL/gVSS/d was obtained at pH = 5.8 and HRT = 32 hours. Moreover, hydrogenase targeted RT-PCR results indicate that Clostridium thermocellum and Klebsiella pneumoniae predominated.

Ornithine decarboxylase prevents methotrexate-induced apoptosis by reducing intracellular reactive oxygen species production.

Methotrexate (MTX), a folate antagonist, was developed for the treatment of malignancies, and is currently used in rheumatoid arthritis (RA) and other chronic inflammatory disorders. It has been proven in short-term and long-term prospective studies that low doses of MTX (0.75 mg/Kg/week) are effective in controlling the inflammatory manifestations of RA. Low-concentrations of MTX achieve apoptosis and clonal deletion of activated peripheral T cells. One of the mechanisms of the anti-inflammatory and immunosuppressive effects may be the production of reactive oxygen species (ROS). However, the drug resistance of MTX in malignancies remains poorly understood. Ornithine decarboxylase (ODC) plays an important role in diverse biological functions, including cell development, differentiation, transformation, growth and apoptosis. In our previous studies, ODC overexpression was shown to prevent TNFalpha-induced apoptosis via reducing ROS. Here, we also investigated one mechanism of MTX-induced apoptosis and of drug resistance as to the anti-apoptotic effects of ODC during MTX treatment. We found MTX could induce caspase-dependent apoptosis and promote ROS generation together with disrupting the mitochondrial membrane potential (DeltaPsim) of HL-60 and Jurkat T cells. Putrescine and ROS scavengers could reduce MTX-induced apoptosis, which leads to the loss of DeltaPsim, through reducing intracellular ROS. Overexpression of ODC in parental cells had the same effects as putrescine and the ROS scavengers. Moreover, ODC overexpression prevented the decline of Bcl-2 that maintains DeltaPsim, the cytochrome c release and activations of caspase 9 and 3 following MTX treatment. The results demonstrate that MTX-induced apoptosis is ROS-dependent and occurs along a mitochondria-mediated pathway. Overexpressed ODC cells are resistant to MTX-induced apoptosis by reducing intracellular ROS production.

Ornithine decarboxylase prevents tumor necrosis factor alpha-induced apoptosis by decreasing intracellular reactive oxygen species.

Ornithine decarboxylase (ODC) plays an essential role in various biological functions, including cell proliferation, differentiation and cell death. However, how it prevents the cell apoptotic mechanism is still unclear. Previous studies have demonstrated that decreasing the activity of ODC by difluoromethylornithine (DFMO), an irreversible inhibitor of ODC, causes the accumulation of intracellular reactive oxygen species (ROS) and cell arrest, thus inducing cell death. These findings might indicate how ODC exerts anti-oxidative and anti-apoptotic effects. In our study, tumor necrosis factor alpha (TNF-alpha) induced apoptosis in HL-60 and Jurkat T cells. The kinetic studies revealed that the TNF-alpha -induced apoptotic process included intracellular ROS generation (as early as 1 h after treatment), the activation of caspase 8 (3 h), the cleavage of Bid (3 h) and the disruption of mitochondrial membrane potential (Delta psi(m)) (6 h). Furthermore, ROS scavengers, such as glutathione (GSH) and catalase, maintained Delta psi(m) and prevented apoptosis upon treatment. Putrescine and overexpression of ODC had similar effects as ROS scavengers in decreasing intracellular ROS and preventing the disruption of Delta psi(m) and apoptosis. Inhibition of ODC by DFMO in HL-60 cells only could increase ROS generation, but did not disrupt Delta psi(m) or induce apoptosis. However, DFMO enhanced the accumulation of ROS, disruption of Delta psi(m) and apoptosis when cells were treated with TNF-alpha . ODC overexpression avoided the decline of Bcl-2, prevented cytochrome c release from mitochondria and inhibited the activation of caspase 8, 9 and 3. Overexpression of Bcl-2 maintained Delta psi(m) and prevented apoptosis, but could not reduce ROS until four hours after TNF-alpha treatment. According to these data, we suggest that TNF-alpha induces apoptosis mainly by a ROS-dependent, mitochondria-mediated pathway. Furthermore, ODC prevents TNF-alpha -induced apoptosis by decreasing intracellular ROS to avoid Bcl-2 decline, maintain Delta psi(m), prevent cytochrome c release and deactivate the caspase cascade pathway.

Imaging cells and tissues with refractive index radiology.

Can individual cells, including live cells, be imaged using hard x rays? Common wisdom until now required sophisticated staining techniques for this task. We show instead that individual cells and cell details can be detected in culture solution and tissues with no staining and no other contrast-enhancing preparation. The sample examined can be much thicker than for many other microscopy techniques without sacrificing the capability to resolve cells. The key factor in our approach is the use of a coherent synchrotron source and of contrast mechanisms based on the refractive index. The first successful tests were conducted on a variety of cell systems including skin and internal leaf cells, mouse neurons, rabbit fibroblast cells, and human tumor cells.

Midazolam attenuates adenosine diphosphate-induced P-selectin expression and platelet-leucocyte aggregation.

BACKGROUND AND OBJECTIVE: The expression of P-selectin on the surface of platelets and platelet-leucocyte conjugate formation are considered to be an indicator of platelet activation in thrombotic and inflammatory disease. Midazolam is a widely used sedative and anaesthetic induction agent. It may inhibit platelet aggregation and suppress interleukin-6 and -8 response in human leucocytes, but any effect on the adhesion of activated platelets to leucocytes remains obscure. We have examined the influence of midazolam on adenosine diphosphate (ADP)-induced platelet surface P-selectin expression and platelet-leucocyte aggregation in whole blood. METHODS: Human whole blood was stimulated with 2 x 10(-5)M ADP in the presence of midazolam (3 x 10(-4) to 3 x 10(-6)M). Samples were stained with a fluorochrome-conjugated CD62P and CD41a antibody for detecting human platelet P-selectin antigens. The leucocyte subpopulations were separately gated and platelet-leucocyte aggregates were defined as cells found positive for CD45 and CD62P. All samples were analysed and were electronically separated into specific cell types (platelets, neutrophils, monocytes and lymphocytes) according to their typical forward/side scattering by flow cytometry. RESULTS: Midazolam significantly inhibited ADP-induced platelet P-selectin expression and attenuated platelet-leucocyte aggregation (mainly in neutrophils and monocytes) in a dose-dependent manner with a maximum inhibitory effect at 3 x 10(-4)M (P < 0.01). CONCLUSIONS: This study demonstrated that midazolam decreases the ADP-induced expression of platelet surface P-selectin and platelet-leucocyte aggregation.

The retina as a novel in vivo model for studying the role of molecules of the Bcl-2 family in relation to MPTP neurotoxicity.

To determine the roles of different members of the family of B cell lymphoma protooncogene (Bcl-2) in relation to neurotoxin-induced neuronal degeneration, the pattern of the expression of a number of molecules of the Bcl-2 family was studied immunocytochemically in the retinas of C57BL/6J mice after intraperitoneal (IP) injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Three days to 12 weeks after MPTP treatment, a detectable reduction of tyrosine hydroxylase immunoreactivity in the amacrine cells was observed, with an increase of Bcl-2 expression in the Müller glial cells, and a de novo expression of Bad and Bax in the retinal ganglion cells, optic nerve fibers and plexiform layers. In contrast, a slight decrease of Bcl-x(L) immunoreactivity in the retinal ganglion cells was observed, whereas Bcl-x(S/L) immunoreactivity was increased slightly in the retinas of MPTP-treated mice compared with that of the controls. In animals that received MPTP injection, an increase in immunostaining of GFAP, glutamine synthetase, and Mac-1 (CD11b) in astrocytes, Müller cells, and microglia was invariably observed, indicating an activation or dysfunction of retinal glial cells. These findings are consistent with the current view that glial dysfunction is important in mediating the cytotoxic effect of a variety of neurotoxic molecules, including MPTP, and that different members of Bcl-2 family may have different roles as far as neuronal degeneration or neuroprotection is concerned.

Electrochemistry: building on bubbles in metal electrodeposition.

In the electrodeposition of metals, a widely used industrial technique, bubbles of gas generated near the cathode can adversely affect the quality of the metal coating. Here we use phase-contrast radiology with synchrotron radiation to witness directly and in real time the accumulation of zinc on hydrogen bubbles. This process explains the origin of the bubble-shaped defects that are common in electrodeposited coatings.

Gamma dose measurement in a water phantom irradiated with the BNCT facility at THOR.

It has been proposed that a LiF thermoluminescence dosemeter (TLD) is used as a gamma dosemeter in a water phantom irradiated with the BNCT facility at THOR. Based on the TLD neutron sensitivity and neutron fluxes in the water phantom, which were simulated by the MCNP code, TLD-700 was chosen as a gamma dosemeter in this report. For the correction of the neutron influence on TLD-700, the thermal neutron sensitivity to TLD-700 was investigated with MCNP simulation and the thermal neutron flux was measured with gold foils using the cadmium difference technique. The correction to the neutron influence on the TLD was established on the TLD thermal neutron sensitivity. the thermal neutron flux, and the conversion factor from energy deposition in the TLD to the TLD response. By comparing the experimental data with the thermal neutron influence correction, these data are in very good agreement with the MCNP predictions.

Sequential up-regulation of the c-fos, c-jun and bax genes in the cortex, striatum and cerebellum induced by a single injection of a low dose of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in C57BL/6 mice.

We investigated whether single injection of 1-methyl-4-phenyl-1,2,3,6- tetrahydropyridine (MPTP) (20 mg/kg) will alter the expression of pro-apoptotic genes, namely, the c-fos, c-jun, and bax, in the striatum, cortex, and cerebellum of adult male C57BL/6 mice using reverse transcription-polymerase chain reaction assay. Injection of MPTP induced a transient decrease in the content of tyrosine hydroxylase estimated by the immunoreactivity in the striatum, which completely recovered 14 day after injection. A rapid but transient up-regulation of c-fos and c-jun genes occurred an hour after MPTP-injection, and a delayed but persistent up-regulation of bax gene expression occurred 3 day after injection. The up-regulation of these genes was present in all the examined brain regions. This result suggests that MPTP, at a low dose causing transient degeneration in the striatum, is capable of triggering two genetic pathways related to the generation of apoptosis in both dopaminergic and non-dopaminergic systems in the mouse brain.

Measurement of high dose rates by photon activation of indium foils.

Photon activation of indium foils is proposed as a dosimetry technique for high dose rate measurements in a 60Co irradiation facility. The irradiated indium nuclei may be raised to its metastable isomers of 113mIn and 115mIn. The isomer 115mIn, with appreciable induced radioactivity, was selected for dose-rate measurements. Based on the photon flux distribution and the derived dose rates, which were simulated by the MCNP code, the dependence of dose rate measurement sensitivity of indium foils with respect to photon energy at various irradiation distances is described. For practical uses, the radioactivity of 115mIn was linearly related to the dose rate response at the specified irradiation positions. By comparing with a calibrated dosimetry system, the measurement deviation of the indium dosimeter, over dose rates ranging from 10 to 10(4) Gy/h, was evaluated and exhibited an uncertainty of +/- 7%. Other related characteristics including measurement sensitivity and range, linearity with respect to the variation of dose rate, and limitations of the indium dosimeter were evaluated to justify it as an alternative for monitoring dose rate in an irradiation field.

Hepatic enzyme induction and acute endocrine effects of 2,2',3,3',4,6'-hexachlorobiphenyl and 2,2',3,4',5',6-hexachlorobiphenyl in prepubertal female rats.

Polychlorinated biphenyls (PCBs) with the liable 2,3,6-substitution are important components of certain commercial mixtures and frequently detected in biota, but little is known about their enzyme induction abilities and possible endocrine-disrupting effects. CB 132 (2,2',3,3',4,6'-hexachlorophenyl) and CB 149 (2,2'3,4',5',6-hexachlorophenyl) were investigated in weanling female rats dosed intraperitoneally on days 21 and 22 and killed on day 24 of age. Uterotropic response, serum thyroid hormone, and hepatic enzyme induction were examined in prepubertal female rats treated with these two environmentally relevant 2,3,6-substituted chlorobiphenyl (CB) congeners from 8 mg/kg to 96 mg/kg. The readily metabolized CB 132 did not cause any significant increase in all endpoints measured in the present study. On the other hand, CB 149 was a weak PROD and BROD inducer and a modest depleter of serum thyroxine in prepubertal female rats. The finding of thyroid hormone disruption by CB 149 may lead to biologically significant neurobehavioral and neurochemical changes in developing animals via milk lactation.

Reduction of sperm motility in a male laboratory worker exposed to solvents: a case study.

A 34-year-old male laboratory worker suffered from asthenospermia and fertility problems. He was suspected of having been exposed to solvents used at work due to a malfunction of the ventilation system in his laboratory from August 1996 to April 1997. A laboratory walk-through and air and bulk sample collection were performed to determine the possible exposure levels of chemical hazards in his job. The scenario was reconstructed to simulate the worker's previous exposure during the ventilation shutdown period. It was found that the worker was possibly exposed to chloroform at levels of 10 or 50 times higher than the permissible exposure limit or the threshold limit value of 2 hr/day, 5.5 days/week, and 4.25 weeks/month for 8 months. Because chloroform is known to be spermatotoxic, the possibility of chloroform causing the worker's asthenospermia cannot be ruled out. Further study on spermatotoxicity of chloroform is warranted.