[Evaluation of short-term effect of intense pulsed light combined with meibomian gland expression in the treatment of meibomian gland dysfunction].

Objective: To explore short-term effect of intense pulsed light (IPL) combined with meibomian gland expression in treating meibomian gland dysfunction (MGD). Methods: This study was a prospective, randomized, double-masked, controlled study. Forty-four MGD patients were enrolled in the study and received three consecutive IPL treatments with an interval of 4 weeks. One eye of each patient was randomly assigned as the study eye receiving the IPL therapy with an energy of 14-16 J/cm(2), and the fellow eye was as the control eye receiving a placebo therapy with 0 J/cm(2). Meibomian gland expression was immediately performed after the IPL treatment in both eyes. Efficacy was evaluated through assessment of the meibomian gland yielding secretion score (MGYSS) , SPEED questionnaire, tear film break-up time (TBUT), cornea fluorescein staining and infrared meibography. Safety was evaluated through best spectacle corrected visual acuity, intraocular pressure, slit lamp examination and fundus examination. These examinations were performed before and after each treatment. Results: Significant improvements were observed in the MGYSS and TBUT after IPL treatments (P<0.05). The improvements compared to the baseline of MGYSS at the upper eyelid in the treatment eyes were significantly higher than those in the control eyes after the first treatment (Z=-2.036, P=0.003). The improvements compared to baseline of MGYSS at the lower eyelid and the TBUT in the treatment eyes were significantly higher than those in the control eyes after the second treatment (Z=-2.999 and -2.036, respectively P=0.007 and 0.042, respectively). SPEED and cornea fluorescein staining were decreased in both eyes after IPL treatments, but there was no statistical difference between the two eyes. No obvious complication was observed in the study. Conclusions: IPL treatment combined with meibomian gland expression is an efficient and safe therapy, and can increase meibomian gland yielding secretion, increase the TBUT, relieve the symptoms and repair the corneal epithelium defects for MGD eyes. (Chin J Ophthalmol, 2017, 53: 675-681).

[The effect of long-term contact lens wear on the morphology of meibomian glands].

OBJECTIVE: To evaluate the effect of long-term contact lens (CL) wear on the morphology of meibomian glands (MGs) using meiboscore and digital analysis. METHODS: Retrospective study. Sixty right eyes of sixty patients were involved in this study, and the data were analyzed retrospectively. According to the duration of CL wear, all patients were divided into three groups, nonwear group (n=21), short-term group (duration of CL wear ≤3 years, n=19) and long-term group (duration of CL wear>3 years, n=20). Digital images of MGs obtained by meibography were analyzed using Image J software, providing the area percentage of MGs loss. The meiboscores were also examined, and the data were analyzed using one-way ANOVA and Kruskal-Wallis test. RESULTS: Ten out of 21 nonwearers were scored 0 point, and 11 were scored 1 point in the upper lid meiboscores, while 7 were scored 0 point, 9 were scored 1 point, and 5 were scored 2 points in the total meiboscores. Seven out of 19 short-term wearers were scored 0 point, 10 were scored 1 point, and 2 were scored 2 points in the upper lid meiboscores, while 5 were scored 0 point, 6 were scored 1 point, 6 were scored 2 points, and 2 were scored 3 points in the total meiboscores. Four out of 20 long-term wearers were scored 0 point, 7 were scored 1 point, and 9 were scored 2 points in the upper lid meiboscores, while 3 were scored 0 point, 4 were scored 1 point, 4 were scored 2 points, 4 were scored 3 points, 4 were scored 4 points, and 1 was scored 5 points in the total meiboscores. The meiboscores of the upper eyelid and total meiboscores among the three groups were significantly different (Hc=9.967, P=0.007; Hc=9.725, P=0.008). The meiboscores of the upper eyelid and total meiboscores were significantly higher in the long-term group compared to the nonwear group (Z=102.500, P=0.003, Z=100.500, P=0.003) and the short-term group (Z=120.500, P=0.050, Z=117.500, P=0.041). No significant difference was found between the short-term group and the nonwear group. The median of the MGs loss area percentage in the upper eyelid of the nonwear, short-term and long-term groups was 9.2%, 13.3% and 16.7%, respectively. The median of the total MGs loss area percentage in the nonwear, short-term and long-term groups were 6.6%, 8.8% and 13.0%, respectively. The above medians were significantly different among the three groups (Hc=6.390, P=0.041; Hc=7.019, P=0.030). They were significantly larger in the long-term wearers than the nonwearers (Z=120.500, P=0.019, Z=120.500, P=0.009). No significant difference was found between the short-term group and the nonwear group, or between the short-term group and the long-term group. No significant differences in the meiboscores or MGs loss area percentage in the lower eyelid were noticed among the three groups. The area under the curve of total area percentage of MGs loss in receiver operating characteristic analysis was 0.981 (P<0.001). CONCLUSIONS: Long-term (more than 3 years) CL wear can cause MGs loss. Digital analysis is helpful in the morphologic evaluation of MGs. (Chin J Ophthalmol, 2016, 52: 604-609).

Short report: increased susceptibility to Plasmodium malariae in pregnant alpha(+)-thalassemic women.

The influence of alpha(+)-thalassemia on malaria in pregnancy was assessed in a cross-sectional study of 530 women in Ghana. Plasmodial infections, alpha(+)-thalassemia, serum levels of C-reactive protein, and antimalarial drugs in urine were determined. The alpha-globin genotypes did not correlate with the prevalence of Plasmodium falciparum-infection and parasite densities. However, Plasmodium malariae tended to be more frequent in alpha(+)-thalassemic women (P = 0.05). Excluding women with residual antimalarials, a significant excess of P. malariae was observed in alpha(+)-thalassemic individuals. Febrile responses (P = 0.05) and inflammation (CRP > 0.6 mg/dl, P = 0.06) appeared to be less common in infected alpha(+)-thalassemic women and were also comparatively rare in parasitemic individuals who harbored double species infections with P. falciparum and P. malariae. Plasmodium malariae may influence the pathogenesis of falciparum malaria leading to a low prevalence of inflammation and febrile responses in alpha(+)-thalassemic women.

Submicroscopic Plasmodium falciparum infections in pregnancy in Ghana.

Malarial parasitaemia below the threshold of microscopy but detectable by polymerase chain reaction (PCR) assays is common in endemic regions. This study was conducted to examine prevalence, predictors, and effects of submicroscopic Plasmodium falciparum infections in pregnancy. In a cross-sectional study among 530 pregnant women in Ghana, plasmodial infections were assessed by microscopy and PCR assays. Concentrations of haemoglobin and C-reactive protein (CRP) were measured and antimalarial drugs (chloroquine, pyrimethamine) in urine were demonstrated by ELISA dipsticks. By microscopy, 32% of the women were found to harbour malaria parasites. This rate increased to 63% adding the results of the parasite-specific PCR. P. falciparum was present in all but one infection. With increasing gravidity, infection rates and parasite densities decreased and the proportions of submicroscopic parasitaemia among infected women grew. Correspondingly, anaemia, fever and evidence of inflammation (CRP > 0.6 mg/dl) were more frequent in primigravidae than in multigravidae. Antimalarial drugs were detected in 65% of the women and were associated with a reduced prevalence of P. falciparum infections and a raised proportion of submicroscopic parasitaemia. Both gravidity and antimalarial drug use were independent predictors of submicroscopic P. falciparum infections. These infections caused a slight reduction of Hb levels and considerably increased serum concentrations of CRP. Conventional microscopy underestimates the actual extent of malarial infections in pregnancy in endemic regions. Submicroscopic P. falciparum infections are frequent and may contribute to mild anaemia and inflammation in seemingly aparasitaemic pregnant women.

Anaemia in pregnant Ghanaian women: importance of malaria, iron deficiency, and haemoglobinopathies.

In sub-Saharan Africa, anaemia in pregnancy results from multiple causes including malaria, iron deficiency and haemoglobinopathies. In a cross-sectional study among 530 pregnant women in Ghana in November-December 1998, red blood cell indices were analysed with respect to malaria, serum concentrations of ferritin and C-reactive protein (CRP), and the haemoglobin and alpha-globin genotypes. Anaemia (haemoglobin [Hb] < 11 g/dL) was found in 54% of the women; 63% harboured malaria parasites at predominantly low numbers. Ferritin levels were considerably influenced by malaria and inflammatory processes (CRP > 0.6 mg/dL). Depending on the definition applied, the prevalence of iron deficiency ranged between 5% and 46%. The HbAS trait was observed in 14%, HbAC and elevated HbF in 7% each, and sickle cell disease in 1%. Heterozygous beta-thalassaemia was present in 1% of the women and alpha(+)-thalassaemia in 33% (29% heterozygous, 4% homozygous). Women with HbAS had higher malaria parasite densities than those with HbAA. In individuals with highly elevated HbF (> 10%), parasitaemia occurred in 27% only. Low gravidity, second trimester of pregnancy, malaria, raised CRP levels, and homozygous alpha(+)-thalassaemia were independent risk factors for anaemia in multivariate analysis. alpha(+)-Thalassaemia, however, was associated with a lesser degree of malarial anaemia when compared to non-thalassaemic women. Iron deficiency appears not to be a major health problem in this population. Haemoglobinopathies are common but, except for homozygous alpha(+)-thalassaemia, do not substantially contribute to anaemia in pregnancy. alpha(+)-Thalassaemia ameliorates malarial anaemia in pregnant women.

[Jugulotympanic glomus tumors: a report of 11 cases].

OBJECTIVE: To evaluate the surgical technique in removal of jugulotympanic glomus tumor. METHODS: Retrospective analysis of surgical techniques and effects of the surgical treated 11 cases (1982-1998) of jugulotympanic glomus tumors (tympanic type I, 1, II, 1, IV, 3; jugular type I, 1, III, 5). RESULTS: The tumors of all 11 patients were removed completely and the wounds healed smoothly. Only one case had postoperative laryngeal nerve paralysis. There was no recurrence after 1-8 years follow-up. CONCLUSION: Suitable surgical techniques are available for removal of jugulotympanic glomus tumors and are chosen according to the size and location of the tumor. Postauricular incision is suitable for Glomous tympanicum Type II, III, IV. Since postauricular incision with superior and inferior extension provides a good exposure of the neck and temporal bone, it is suitable for surgical removal of Glomus jugulare type I. In case of Glomus jugulare type III, postauricular large "C" incision may be chosen for resection of the mid- and infra-temporal fosse, neck and skull base tumor.

HSV-1-inducible proteins bind to NF-kappa B-like sites in the HSV-1 genome.

Several putative NF-kappa B-binding sites in the ICP0 and Vmw65 herpes simplex virus type-1 (HSV-1) genes have been identified. Oligonucleotides encoding some of these sites bind specifically to purified NF-kappa B protein and an NF-kappa B-like protein in nuclear extracts of phorbol ester- or cycloheximide-induced human embryonic lung (HEL) cells. HSV-1 infection of HEL cells induced a nuclear factor that binds specifically to kappa B sites in the ICP0 and Vmw65 gene regions and comigrates with complexes formed by purified NF-kappa B. The HSV-1-inducible nuclear factor bound to the authentic immunoglobulin (Ig) kappa B site. Transient expression of chloramphenicol acetyltransferase (CAT) plasmids containing two copies of the Ig kappa B site upstream of the c-fos promoter (kappa B2-CAT) showed activity in HEL cells. HSV-1 infection of kappa B2-CAT-transfected HEL cells, however, induced a dramatic increase in CAT activity; mutation in the NF-kappa B-binding site of kappa B2-CAT abolished the inducibility of CAT gene expression. Our results demonstrate that the HSV-1 ICP0 and Vmw65 gene regions contain binding sites for NF-kappa B, and that HSV-1-inducible proteins bind to NF-kappa B-like sites in the HSV-1 genome.

Detection of herpes simplex virus thymidine kinase and latency-associated transcript gene sequences in human herpetic corneas by polymerase chain reaction amplification.

Herpes simplex virus (HSV) latency in sensory ganglion neurons is well documented, but the existence of extraneuronal corneal latency is less well defined. To investigate the possibility of extraneuronal latency during ocular HSV infection, corneal specimens from 18 patients with quiescent herpes simplex keratitis (HSK) were obtained at the time of keratoplasty. Polymerase chain reaction (PCR) amplification followed by southern blot hybridization with a radiolabeled oligonucleotide probe was done to detect the presence of HSV-1 genome in these human corneal samples. Two pairs of oligonucleotides from the region of the HSV thymidine kinase (TK) gene and the latency-associated transcript (LAT) gene were used as primers in the PCR amplification. The DNA sequences from either the TK or the LAT gene were identified in 15 of 18 HSK corneas (83%). These results demonstrate that the HSV genome was retained, at least in part, in human corneas during quiescent HSV infection, giving further support to the concept of corneal extraneuronal latency.

Extraneuronal herpetic latency: animal and human corneal studies.

HSV DNA has been previously detected by both in situ and dot blot hybridization in neuronal tissues latently infected with herpes simplex virus (HSV), but not in extraneuronal tissues. The present study, using dot blot hybridization with a cloned full-length HSV DNA probe and subtractive hybridization assays for detecting HSV RNA, reveals both the presence and activity of the HSV genome in 100% of HSV latently infected rabbit corneas tested. Studies on human herpetic corneas taken at keratoplasty using slot blot hybridization with a cloned full-length HSV DNA probe demonstrated positive binding (hybridization) to the probe in 50% of samples tested but no binding to normal human control DNA. These studies confirm earlier, less sensitive virus recovery assays and implicate the cornea as an extraneuronal site of HSV latency and reactivation.

Molecular analysis of acyclovir-induced suppression of HSV-1 replication in rabbit corneal cells.

An in vitro HSV drug-suppression model has been established in rabbit corneal cell (SIRC) monolayers. Confluent SIRC monolayers were inoculated with McKrae strain HSV-1 (0.014 PFU/cell) and subsequently suppressed with acyclovir (ACV) (40 micrograms/ml) after adsorption for 1 hr at 37 degrees C. On days 0-5 postinoculation (PI), infectious HSV-1 was detected in approximately 50% of the SIRC cell cultures by standard supernatant and cell-free homogenate co-culture assays. On days 6-10 postsuppression, infectious HSV was detected in only 7-19% of the cultures. After removal of ACV suppression in the cultures (day 11 PI), HSV cytopathology developed to a 3-4+ level within 2-5 days. Dot blot hybridization of DNA extracted from the cultures indicated that the HSV genome was retained consistently in SIRC cells at a level of 0.0015-0.015 copies per cell during active ACV-suppression. During ACV-suppressed infection, approximately 0.9% of the SIRC cells contained the HSV genome as demonstrated by blot hybridization. After removal of ACV, a 1000-fold increase in HSV DNA concentration in SIRC cell cultures was detected.

Varicella-zoster virus infection of human sensory neurons.

Primary varicella-zoster virus (VZV) infection of humans may result in latent infection of sensory neurons in the peripheral nervous system. To examine the interaction of VZV with the sensory neuron we infected immunochemically defined human neurons with cell-associated VZV. Utilizing double-label immunofluorescence technology, a VZV-specific glycoprotein and a nonglycosylated phosphoprotein were detected in human fetus dorsal root ganglion (DRG) neurons, as defined by the presence of the neuron-specific enolase isoenzyme and the A2B5 ganglioside antigen, respectively. In addition to VZV antigen expression, progressive virus-induced cytopathic damage (neuronal enlargement and nuclear granulation of a fraction of the neuron population) was evident. As determined by transmission electron microscopy, VZV-infected human fetus DRG neurons contained empty and complete nucleocapsids with numerous pleomorphic virus particles in the cytoplasm, often in association with vacuoles. Although virus-specific antigen expression, particle synthesis, and cytopathic effects were observed in the human neuron population, neurons were less susceptible to VZV-induced cytopathic damage than supporting nonneuronal cells, suggesting neuronal modulation of VZV infection in vitro. This system provides the first model to examine the neuron- and virus-specific gene(s) and gene product(s) pertinent to the interaction of VZV with the human neuron.