Postoperative Onset and Detection of SARS-CoV-2 in Surgically Resected Specimens From Gastrointestinal Cancer Patients With Pre/Asymptomatic COVID-19.

OBJECTIVE: To describe the epidemiologic features and clinical courses of gastrointestinal cancer patients with pre/asymptomatic COVID-19 and to explore evidence of SARS-CoV-2 in the surgically resected specimens. SUMMARY BACKGROUND DATA: The advisory of postponing or canceling elective surgeries escalated a worldwide debate regarding the safety and feasibility of performing elective surgical procedures during this pandemic. Limited data are available on gastrointestinal cancer patients with pre/asymptomatic COVID-19 undergoing surgery. METHODS: Clinical data were retrospectively collected and analyzed. Surgically resected specimens of the cases with confirmed COVID-19 were obtained to detect the expression of ACE2 and the presence of SARS-CoV-2. RESULTS: A total of 52 patients (male, 34) with a median age 62.5 years were enrolled. All the patients presented no respiratory symptoms or abnormalities on chest computed tomography before surgery. Six patients (11.5%) experienced symptom onset and were confirmed to be COVID-19. All were identified to be preoperatively pre/asymptomatic, as 5 were with SARS-CoV-2 presenting in cytoplasm of enterocytes or macrophages from the colorectal tissues and 1 had symptom onset immediately after surgery. The case fatality rate in patients with COVID-19 was 16.7%, much higher than those without COVID-19 (2.2%). CONCLUSIONS: Gastrointestinal cancer patients with pre/asymptomatic COVID-19 were at high risk of postoperative onset and death. At current pandemic, elective surgery should be postponed or canceled. It highlights the need for investigating the full clinical spectrum and natural history of this infection. The early colorectal tropism of SARS-CoV-2 may have major implications on prevention, diagnosis, and treatment of COVID-19.

4-Phenylbutyric Acid Attenuates Endoplasmic Reticulum Stress-Mediated Intestinal Epithelial Cell Apoptosis in Rats with Severe Acute Pancreatitis.

OBJECTIVES: The present study aimed to determine whether intestinal epithelial cell (IECs) apoptosis could be induced by endoplasmic reticulum stress (ERS) in severe acute pancreatitis (SAP), and the role of chemical chaperone 4-phenylbutyric acid (4-PBA) in SAP-associated intestinal barrier injury. METHODS: Twenty-four male Sprague Dawley rats were randomly divided into three groups: the sham operation group, the SAP group, and the SAP model plus 4-PBA treatment group (4-PBA group). A rat model of SAP was induced by retrograde injection of 5% sodium taurocholate (STC) into the biliopancreatic duct; in the 4-PBA group, 4-PBA was injected intraperitoneally at a dose of 50 mg/kg body weight for 3 days before modeling. RESULTS: The results indicated that 4-PBA attenuated the following: (1) pancreas and intestinal pathological injuries, (2) serum TNF-α, IL-1ß, and IL-6, (3) serum DAO level, serum endotoxin level, (4) the apoptosis of IECs, (5) ER stress markers (caspase-12, CHOP, GRP78, PERK, IRE1α, ATF6) and caspase-3 expression in intestinal. However, the serum AMY, LIPA levels, and the expression of caspase-9, caspase-8 were just slightly decreased. CONCLUSIONS: ERS may be considered a predominant pathway, which is involved in the apoptosis of IECs during SAP. Furthermore, 4-PBA protects IECs against apoptosis in STC-induced SAP by attenuating the severity of ERS.

Inhibition of endoplasmic reticulum stress by 4-phenylbutyric acid prevents vital organ injury in rat acute pancreatitis.

This study was conducted to investigate the effect of 4-phenylbutyric acid (4-PBA) on vital organ injury following sodium taurocholate-induced acute pancreatitis (AP) in rats and the pertinent mechanism. The serum biochemical indicators and key inflammatory cytokines, histopathological damage and apoptosis of vital organs in rat AP, were evaluated in the presence or absence of 4-PBA. Moreover, mRNA and protein levels of endoplasmic reticulum stress (ERS) markers were assessed. 4-PBA significantly attenuated the structural and functional damage of vital organs, including serum pancreatic enzymes, hepatic enzymes, creatinine, and urea. The morphological changes and infiltration of neutrophils and macrophages were reduced as well. These effects were accompanied by decreased serum levels of proinflammatory TNF-α and IL-1ß. Furthermore, 4-PBA diminished the expression of ERS markers (glucose-regulated protein 78, CCAAT/enhancer-binding protein homologous protein, protein kinase R-like ER kinase, activated transcription factor 6, and type-1 inositol requiring enzyme) in vital organs of AP rats. 4-PBA also reduced AP-induced apoptosis in lung, liver, and kidney tissues as shown by TUNEL assay. The present study demonstrated that 4-PBA protected pancreas, lung, liver, and kidney from injury in rat AP by regulating ERS and mitigating inflammatory response to restrain cell death and further suggested that 4-PBA may have potential therapeutic implications in the disease. NEW & NOTEWORTHY In this study, we suggest that endoplasmic reticulum stress (ERS) is an important player in the development of acute pancreatitis-induced multiorgan injury, providing additional evidence for the proinflammatory role of ERS. Because 4-phenylbutyric acid has been suggested to inhibit ERS in many pathological conditions, it is possible that this effect can be involved in alleviating inflammatory response and cell death to ameliorate vital organ damage following acute pancreatitis induced by sodium taurocholate in rats.

Serum thyroid hormones levels are significantly decreased in pregnant rats with acute pancreatitis.

Acute pancreatitis in pregnancy (APIP), which was thought to be a rare but severe disease, with a high perinatal mortality among maternal-fetuses. Our research aimed to study and assess thyroid injury in a rat model of APIP and its possible mechanisms. The APIP model was established by retrograde injection with sodium taurocholate. Sham-operated (SO) and APIP groups were performed at 3 time-points. Histological changes in the maternal thyroid and pancreas were assessed. The activities of serum amylase, lipase and levels of FT3, FT4, MDA, TNF-α and IL-1ß were detected in maternal rats, and the expression of MIF, ICAM-1 and CD68 in the maternal thyroids were determined. In this study, maternal thyroid injury as well as pancreas injury occurred in a time-dependent manner. The activities of serum amylase, lipase and levels of MDA, TNF-α and IL-1ß were markedly increased in acute pancreatitis rats, the levels of serum FT3 and FT4 were obviously decreased in APIP groups, and the expressions of MIF, ICAM-1 and CD68 were significantly increased in the thyroid of the APIP group. Ultrastructural thyroid injuries were observed in the APIP group. Our research suggests that thyroid injury is involved in the rat experimental model of APIP. The degree of thyroid dysfunction is associated with APIP, which may affect the prognosis of acute pancreatitis.

Hydrogen-rich saline attenuates acute renal injury in sodium taurocholate-induced severe acute pancreatitis by inhibiting ROS and NF-κB pathway.

Hydrogen (H2), a new antioxidant, was reported to reduce (•)OH and ONOO(-) selectively and inhibit certain proinflammatory mediators to product, without disturbing metabolic redox reactions or ROS involved in cell signaling. We herein aim to explore its protective effects on acute renal injury in sodium taurocholate-induced acute pancreatitis and its possible mechanisms. Rats were injected with hydrogen-rich saline (HRS group) or normal saline (SO and SAP group) through tail intravenously (6 mL/kg) and compensated subcutaneously (20 mL/kg) after successful modeling. Results showed that hydrogen-rich saline attenuated the following: (1) serum Cr and BUN, (2) pancreatic and renal pathological injuries, (3) renal MDA, (4) renal MPO, (5) serum IL-1ß, IL-6, and renal TNF-α, HMGB1, and (6) tyrosine nitration, IκB degradation, and NF-κB activation in renal tissues. In addition, it increased the level of IL-10 and SOD activity in renal tissues. These results proved that hydrogen-rich saline attenuates acute renal injury in sodium taurocholate-induced acute pancreatitis, presumably because of its detoxification activity against excessive ROS, and inhibits the activation of NF-κB by affecting IκB nitration and degradation. Our findings highlight the potential value of hydrogen-rich saline as a new therapeutic method on acute renal injury in severe acute pancreatitis clinically.

[Expression of PARP/NF-κB and intervention effect of 5-AIQ/PDTC in SAP rats with adrenal damage].

OBJECTIVE: To explore the expression of poly (ADP-ribose) polymerase/nuclear factor-κB (PARP/NF-κB) and intervention effect of 5-aminoisoquinolinone/pyrrolidine dithiocarbamate (5-AIQ/PDTC) in severe acute pancreatitis (SAP) rats with adrenal damage. METHODS: The primarily cultured adrenocortical cells were quantitatively divided into control group (SO), pancreatitis group (SAP), PDTC drug control group (SO+PDTC), PDTC intervention group (SAP+PDTC), 5-AIQ drug control group (SO+ 5-AIQ) and 5-AIQ intervention group (SAP+5-AIQ). The SAP and 2 intervention groups were stimulated with the sera of SAP rats. Then corresponding drugs were added and culture continued for 12 hours. The corticosterone levels and PARP/NF-κB expression were observed for each group. RESULTS: Adrenal cells in vitro cultured were round or oval, had secretory granules and could be stained by 3ß-hydroxysteroid dehydrogenase antibody. The adherence rate was 60% after 48-hour culturing. The corticosterone level of SAP group was significantly lower than that of SO group [ (216.4 ± 15.7) vs (294.8 ± 16.3) µg/L, P < 0.05]. The 2 intervention groups were (258.6 ± 19.0) and (264.3 ± 18.2) µg/L respectively. These two values were higher than those of SAP group (P < 0.05), but lower than those of SO group (P < 0.05). With regards to the expression of PARP-1, the SAP and PDTC intervention groups were higher than SO group while 5-AIQ intervention group was significantly lower than SAP and PDTC intervention groups, but higher than SO and drug control groups. The expression of NF-κB in SAP group was higher than that in SO group. Two intervention groups were lower than SAP group, but higher than SO and drug control groups. CONCLUSION: The pathway of PARP/NF-κB participates in adrenal damage of SAP rats. To a certain extent, the uses of 5-AIQ and PDTC may alleviate adrenal damage.

[Applications of optical coherence tomography in glaucoma].

As one of the most common irreversible eye diseases, early diagnosis and treatment of glaucoma is vital for a good prognosis but difficult in clinical practice. Optical coherence tomography (OCT) is a non-invasive procedure that can quickly acquire high-resolution cross-sectional images of the ocular structure and is used widely in ophthalmic clinics. In terms of glaucoma, OCT is used to measure the thickness of the retinal nerve fiber layer, the structure of the optic disc, the loss of retinal ganglion cells, the parameters of anterior chamber and anterior chamber angle, the thickness of the iris, the thickness of the lens, the thickness of the choroid, the structure of the filtration bleb and so on. This review summarized the clinical application of OCT in glaucoma diagnosis and the evaluation of glaucoma treatment up till now.

Astrocyte polarization in glaucoma: a new opportunity.

Astrocyte polarization is a new concept which is similar to microglia polarization and in which astrocytes are classified as A1 (neurotoxic) and A2 (neuroprotective). Several studies on astrocyte polarization have focused mainly on neurodegenerative diseases, trauma, and infections. However, the role of astrocyte polarization in glaucoma, a neurodegenerative disease, has not been fully explored. In this review, we first describe the characteristics of astrocyte astrogliosis in glaucoma, including morphological, molecular, proliferative and functional changes. We then summarize understanding of astrocyte polarization in other diseases, and show that A1 astrocytes are involved in the death of retinal ganglion cells in glaucoma, and that their neurotoxins kill only damaged retinal ganglion cells. Based on this, we propose new interesting conjecture on astrocyte polarization in glaucoma: (1) That the neurotoxin from A1 astrocytes is a product of the complement system (membrane-attacking complex), since this system is known to mediate synaptic elimination and the C3 expression is clearly increased in A1 astrocytes; (2) that reactive scar-forming astrocytes in the optic nerve head may be classified as A2 astrocytes since their ablation leads to a worse prognosis in glaucoma. Finally, current therapeutic research progress on astrocyte polarization in other diseases is also addressed. Regulation of astrocyte polarization can be achieved by extracellular microglia-related and intracellular pathways. Reduced A1 or increased A2 astrocytes can rescue the nerve. For example, glucagon-like peptide-1 receptor agonist rescues retinal ganglion cells by reducing A1 astrocytes via the extracellular microglia-related pathway in an ocular hypertension model, suggesting that regulation of astrocyte polarization as a therapeutic target in glaucoma is feasible.

Interleukin-4 promotes microglial polarization toward a neuroprotective phenotype after retinal ischemia/reperfusion injury.

Glaucoma results from irreversible loss of retinal ganglion cells (RGCs) through an unclear mechanism. Microglial polarization and neuroinflammation play an important role in retinal degeneration. Our study aimed to explore the function of microglial polarization during glaucoma progression and identify a strategy to alleviate retinal neuroinflammation. Retinal ischemia/reperfusion injury was induced in C57BL/6 mice. In a separate cohort of animals, interleukin (IL)-4 (50 ng/mL, 2 µL per injection) or vehicle was intravitreally injected after retinal ischemia/reperfusion injury. RGC loss was assessed by counting cells that were positive for the RGC marker RNA binding protein, mRNA processing factor in retinal flat mounts. The expression of classically activated (M1) and alternatively activated (M2) microglial markers were assessed by quantitative reverse transcription-polymerase chain reaction, immunofluorescence, and western blotting. The results showed that progressive RGC loss was accompanied by a continuous decrease in M2 microglia during the late phase of the 28-day period after retinal ischemia/reperfusion injury. IL-4 was undetectable in the retina at all time points, and intravitreal IL-4 administration markedly improved M2 microglial marker expression and ameliorated RGC loss in the late phase post-retinal ischemia/reperfusion injury. In summary, we observed that IL-4 treatment maintained a high number of M2 microglia after RIR and promoted RGC survival.

Patients' experience of living with glaucoma: a phenomenological study.

AIM: To explore the life experiences of those living with glaucoma and describe their strategies to deal with the consequences of this disorder. BACKGROUND: Glaucoma, the second most common cause of worldwide blindness, often imposes limitations on the daily functions of its victims, thus resulting in a decline in their quality of life and high costs in healthcare. METHODS: A hermeneutical phenomenological research approach was adopted. Fourteen people with glaucoma were selected for in-depth interviews, and another ten were interviewed in two focus groups. Participants were recruited from a specialized eye hospital in Shanghai. The data were collected from July to September 2009. An interpretive analysis of the data was performed. FINDINGS: The core theme was identified while interpreting the data on the patients' life experiences as 'learning to living with glaucoma' by one of our participants. The meaning of this is demonstrated in four interwoven themes: (1) seeking support; (2) coping with everyday tasks; (3) living with future uncertainties; and (4) adapting to the declined quality of life. CONCLUSION: This paper provides an insight into the living experiences of the patients with glaucoma using 1-on-1 and focus-group interviews, suggesting that the latter can also offer a means of phenomenological inquiry. We found that those with glaucoma can experience uncertainty surrounding treatment, illness prognosis and family members' risk status. In addition, the Chinese culture can influence the patients' strategies of maintaining a healthy lifestyle. In helping those with glaucoma considerations should be taken towards the feelings of future uncertainty that may develop.

[Study on changes of intraocular pressure within 24 hours in primary open angle glaucoma and normal eyes].

OBJECTIVE: To analyze the discipline of intraocular pressure (IOP) variation, through circadian intraocular pressure monitoring in primary open-angle glaucoma (POAG) patients and normal controls, with a view to provide basis for individualized treatment of glaucoma. METHODS: Subjects were enrolled from the outpatients of Shanghai Beizhan Hospital and Eye and ENT Hospital of Fudan University, which were diagnosed as primary open angle glaucoma, from April 2006 to April 2009. Totally there were 102 cases of patients and 83 cases of normal volunteers. All the subjects accepted 24-hour IOP measurements using non-contact tonometer every two hours starting from 8:00 am. And the IOP between 00:00 to 06:00 am was measured in sitting position immediately after wake up. RESULTS: The differences of peak IOP [(16.0 ± 2.7) mm Hg of right eye and (16.2 ± 2.7) mm Hg of left eye in normal group; (25.3 ± 5.6) mm Hg of right eye and (24.8 ± 5.1) mm Hg of left eye in POAG group], valley IOP (11.1 ± 2.5) mm Hg of right eye and (11.0 ± 2.3) mm Hg of left eye in normal group; (16.3 ± 3.7) mm Hg of right eye and (16.2 ± 3.3) mm Hg of left eye in POAG group, average IOP (13.4 ± 2.5) mm Hg of right eye and (13.4 ± 2.5) mm Hg of left eye in normal group; (19.9 ± 4.3) mm Hg of right eye and (19.8 ± 3.8) mm Hg of left eye in POAG group), and IOP fluctuations (5.0 ± 1.6) mm Hg of right eye and (5.2 ± 1.7) mm Hg of left eye in normal group; (9.1 ± 3.6) mm Hg of right eye and (8.6 ± 3.8) mm Hg of left eye in POAG group between two groups were all of statistically significance (P < 0.01). Notably, the peak IOP of 59.6% in normal control group and 73.5% in POAG group were outside working hours, especially in the time period from 00:00 to 06:00 am. The peak value of 50% in normal group and 64.7% in POAG group located between 00:00 to 06:00 in the morning. CONCLUSIONS: By comparison and analysis, 24-hour intraocular pressure measurement could provide us pre-treatment basic state, so as to provide detailed information for individualized treatment. If possible, it is suggested that 24-hour IOP monitoring should be added as a routine examination of primary open angle glaucoma.

[Present status on studies of differentiation into retinal neurons and pigmented cell from induced pluripotent stem cells].

Somatic cells could be induced into pluripotent stem (iPS) cells through transferring special genes (Oct4, Sox2, c-myc and Klf4). This has brought a revolutionary change in stem cell study and application. The generation of iPS cells has great potential and enormous significance as it can resolve some insurmountable problems in stem cells research, such as ethical dilemma, immune rejection, etc. Because of these characteristics, it plays an important role in the repair of various tissues and organs. Rapid progress in this field during the past 3 years convinced us that iPS cells will be more and more applicable in tissue engineering. The present paper reviews the progress of pre-clinical study on iPS cells in the treatment of retinal and optic nerve diseases.

Inhibition of macrophage migration inhibitory factor prevents thyroid dysfunction in pregnant rats with acute pancreatitis.

Acute pancreatitis during pregnancy (APIP) rarely occurs but may lead to preterm delivery and be associated with high fetal mortality. Macrophage migration inhibitory factor (MIF) participates in various inflammatory diseases as a pro-inflammatory cytokine. In this study, we aimed to explore the effects of (S, R)-3-(4-hydroxyphenyl)-4, 5dihydro-5-isoxazole acetic methyl ester (ISO-1), an inhibitor of MIF, on maternal thyroid injury associated with APIP and its potential mechanisms in a pregnant rat model. APIP model was induced by retrograde injection of sodium taurocholate. ISO-1 was injected intraperitoneally 30 min before model establishment. The severity of pancreatitis was assessed by levels of tumor necrosis factor (TNF)­α, interleukin (IL)­1ß, IL-6 of maternal serum as well as histopathological score. Thyroid injury was determined by free triiodothyronine (FT3), free tetraiodothyronine (FT4) and thyroid histopathological score. Levels of MIF in maternal serum and the expression of MIF, CD68, CD3 and intercellular cell adhesion molecule-1 (ICAM-1) as well as oxidative stress status in maternal thyroid tissues were detected. Ultrastructure of maternal thyroid tissues was observed by transmission electron microscope. Thyroid injuries occurred in APIP and the lesions were attenuated with the pretreatment of ISO-1. Moreover, ISO-1 reduced the expression of MIF, attenuated the activations of CD68, CD3, ICAM-1 while improved oxidative stress status in maternal thyroid. Our research suggested a protective role of ISO-1 on thyroid injury and endocrine disorder during APIP, which may be associated with the inhibition of biological functions of MIF.

Cyclic stretch upregulates SDF-1alpha/CXCR4 axis in human saphenous vein smooth muscle cells.

Cyclic stretch (CS) mediates different cellular functions in vascular smooth muscle cells and involves in neointimal hyperplasia and subsequent atherosclerosis of vein grafts. Here, we investigated whether CS can modulate stromal cell-derived factor-1alpha (SDF-1alpha)/CXCR4 axis in human saphenous vein smooth muscle cells. We found CS induced the upregulation of SDF-1alpha and CXCR4 in human saphenous vein smooth muscle cells in vitro, which was dependent on PI3K/Akt/mTOR pathway. Furthermore, CS augmented human saphenous vein smooth muscle migration and focal adhesion kinase (FAK) activation by PI3K/Akt/mTOR pathway. Interestingly, the upregulation of SDF-1alpha/CXCR4 axis was instrumental in CS-induced saphenous vein smooth muscle cell migration and FAK activation, as showed by AMD3100, an inhibitor of SDF-1alpha/CXCR4 axis, partially but significantly blocked the CS-induced cellular effects. Thus, those data suggested SDF-1alpha/CXCR4 axis involves in CS-mediated cellular functions in human saphenous vein smooth muscle cells.

[Trabeculotomy on primary congenital glaucoma: a retrospective study of 164 cases (257 eyes)].

OBJECTIVE: To study the relationship of long-term effect of trabeculotomy on primary congenital glaucoma and the related risk factors. METHOD: 164 consecutive patients with primary congenital glaucoma (257 eyes), underwent initial surgery of trabeculotomy between 1996 and 2007. Follow-up was conducted for 30.9 (8.6 - 58.3) months, with a follow-up rate of 89.02%. Multivariate analysis by Logistic regression was conducted to analyze the relation of the factors including age of onset, time between onset and operation, preoperative intraocular pressure, clarity of cornea, and corneal diameter to the failure of surgery. Cox proportional hazards regression modeling was used to analyze the factors related to success of surgery. RESULT: Multivariate logistic regression showed that the preoperative intraocular pressure (IOP) and clarity of cornea were independent risk factors for final outcome (OR(IOP) = 1.408, P = 0.047, and OR(CLA) = 1.691, P = 0.019). Cox regression showed that clarity of cornea was the factor related to the surgery success time (OR(CLA) = 1.632, P = 0.008). CONCLUSION: Clarity of cornea reflexes the condition of primary congenital glaucoma more stably than IOP. It is possible to prognosticate the surgical outcome to combine the clarity of cornea with the IOP value before operation.

[Changes of neuroglia cells in human glaucoma and animal model of experimental glaucoma].

Glaucoma is one of the major ocular diseases that lead to blindness. It is characterized by optic disk cupping and visual field loss. Glaucoma is a multifactorial group of diseases with many different causes but one common endpoint, progressive loss of retinal ganglion cells. Hence most studies of glaucoma focused on retinal ganglion cells and their nosogenesis. But recent studies have showed that neuroglia cells, as another major kind of cells of nerve system, also undergo an activation process in glaucoma. Their activation is closely connected with the changes of retinal ganglion cells as well as the development of the disease. Therefore, more and more attention is focused on the changes of these cells. This review is a summary about the recent studies on the pathological changes of these four different kinds of neuroglia cells in human glaucoma and in several animal models of experimental glaucoma.

[Progress of research on quality of life of glaucoma patients].

Glaucoma is a kind of long life disease characterized by irreversible optic nerve damage, visual field impairment, and visual acuity loss. Both the disease and its medical management could make the patient perceive difficulties in their daily life activities and social function. Therefore, their quality of life would be affected significantly. This report briefly reviews the recent researches on the quality of life and its influencing factors of glaucoma patients. The researches on how to improve the quality of life of glaucoma patients are also reviewed.

[Construction of CNTF-GFP plasmid and transfection of Schwann cells by electroporation].

OBJECTIVE: To enhance the neurotrophic effect of Schwann cells, promote optic nerve regeneration, and simplify the means of observation, the CNTF-GFP fusion plasmid was constructed and transferred into Schwann cells by electroporation. METHODS: It was an experimental study. Plasmid pcDNA3. 1/CNTF-GFP was constructed and verified by auto-sequence. Cultured Schwann cells were transfected by electroporation. The transfection efficiency was counted by flow cytometry, the transcription of the gene was evaluated by RT-PCR, and the expression of protein was observed by fluorescence microsphere and cell immunofluorescence. RESULTS: CNTF-GFP plasmid was verified correctly. After electroporation, the green fluorescence of gene-transfected Schwann cells can be seen at 3 hours later, increased at 12 hours later, reached the peak during 24 h to 72 h later, and still could be seen at 7 days later. The transfection efficiency was evaluated at 44.93% +/- 12.92% by flow cytometry. The transcription of CNTF gene and the expression of CNTF protein have been proven by RT-PCR and cell immunofluorescence. CONCLUSIONS: CNTF-GFP plasmid was constructed correctly and Schwann cells were transfected by electroporation successfully and CNTF-GFP fusion protein can be expressed well, which became a good foundation for our future's study on the transplantation of gene-modified Schwann cells to promote optic nerve regeneration.

[Clinical analysis on sixteen cases of Sturge-Weber syndrome-associated glaucoma].

OBJECTIVE: To investigate the clinical features of Sturge-Weber syndrome-associated glaucoma and its surgical treatment. METHODS: A retrospective case series study. The general clinical data and related ocular manifestations in 16 patients (21 eyes) with Sturge-Weber syndrome-associated glaucoma in our hospital from January 2003 to December 2007 were analyzed retrospectively. RESULTS: Age of the patients ranged between 1 month to 31 years old, and the median age was 11 years. Bilateral facial angiomas were present in 8 patients, and two of them had extensive hemangioma. Eleven cases had unilateral glaucoma and 3 of them had bilateral facial angiomas. Five patients had bilateral glaucoma and all of them had bilateral facial angiomas. Open anterior chamber angle was found in all affected eyes by gonioscopy. B-scan ultrasonography was performed in 21 eyes and diffused occupying lesions in the choroid were found in 8 eyes (38.1%). Posterior bowing of the iris, low echo in ciliary body and shallow ciliary body detachment were found by ultrasound biomicroscopy. Anti-glaucoma surgeries including trabeculotomy, trabeculectomy, non-penetrating deep sclerectomy, valve implantation and cyclocryotherapy were performed in 18 eyes. Eighty percent of the eyes which underwent trabeculectomy developed choroidal detachment after operation. Ten patients (11 eyes) were followed-up for 22 months on average. Intraocular pressure was significantly lower than that before the operation (t = 5.3956, P < 0.01). Intraocular pressure in all followed-up eyes was controlled at < or = 21 mm Hg (1 mm Hg = 0.133 kPa). CONCLUSIONS: The clinical features of Sturge-Weber syndrome-associated glaucoma include facial angiomas, open anterior chamber angle and choroidal hemangioma. Anti-glaucoma surgery can reduce the intraocular pressure effectively.

Efficacy of low-energy selective laser trabeculoplasty on the treatment of primary open angle glaucoma.

AIM: To investigate the efficacy of low-energy selective laser trabeculoplasty (SLT) on the treatment of primary open angle glaucoma (POAG) patients. METHODS: Outpatients with POAG who underwent 360-degree SLT using an initial energy of 0.3 mJ (total energy of 30-40 mJ) were reviewed retrospectively from September 2011 to January 2018. RESULTS: Eight-six eyes of 44 POAG patients underwent 360-degree SLT using initial energy of 0.3 mJ and were followed up regularly. The total energy used was 32.5±2.5 mJ (23-40 mJ, 105±6 spots). The average pretreatment intraocular pressure (IOP) was 19.8±3.9 mm Hg. At 1, 3, 6mo, 1, and 2y, the post-SLT IOPs (mm Hg) were 16.9±3.3, 16.5±3.3, 17.1±3.4, 16.6±3.5, 16.5±2.8, which were significantly lower than that before treatment (P<0.001). The patients in the SLT success group were found to be younger than those in the SLT failure group. After SLT, 59 eyes that maintained pretreatment medications were defined as the drug retention group. The pre-SLT IOP was 20.1±3.7 mm Hg. At 1, 3, 6mo, 1, and 2y, the post-SLT IOPs (mm Hg) were 17.3±3.6, 16.6±3.5, 17.2±3.6, 16.9±3.8 and 16.5±2.9, respectively. Twenty-seven eyes that required reduced drugs were defined as the drug reduction group. The pre-SLT IOP was 19.2±4.4 mm Hg. At 1, 3, 6mo, 1, and 2y, the post-SLT IOPs (mm Hg) were 16.1±2.6, 16.5±3.1, 16.8±2.9, 16.0±2.6 and 16.3±2.4, respectively. Compared with the pretreatment IOPs, the post-SLT IOPs were significantly lower in drug retention group and drug reduction group. The patients in the drug reduction group were found to be younger than those in the drug retention group. CONCLUSION: Low-energy SLT is safe and effective for POAG patients during a 2-year follow-up. Younger POAG patients may obtain better results after low-energy SLT treatment.