Nutrient dynamics in the Bohai and North Yellow seas from seasonal to decadal scales: Unveiling Bohai Sea eutrophication mitigation in the 2010s.

The eutrophication status in the central Bohai Sea tends to be mitigated in recent years. To explore the recent nutrient status, seasonal surveys were carried out from 2018 to 2021, covering both the Bohai Sea and the adjacent North Yellow Sea. In recent cold seasons, both dissolved inorganic nitrogen concentration (DIN) and the ratio of DIN to soluble reactive phosphorus were lower than those in 2016. In warm seasons, the variations in nutrients and apparent oxygen utilization were correlated with each other, roughly following the traditional Redfield ratio of N:P:O2 of approximately 16:1:(-138). When historical data for N*, which is the excess DIN related to soluble reactive phosphorus, was collated, the Bohai Sea showed a decreasing trend for N* at a rate of -0.64 ± 0.12 µmol N* kg-1 a-1 between 2011 and 2021. During the same period, the North Yellow Sea N* concentrations (i.e., the oceanic end-member of the Bohai Sea N* dynamics) and the local atmospheric nitrogen (N) deposition (atmospheric end-member) were estimated to decline at rates of -0.22 ± 0.04 µmol N* kg-1 a-1 and - 0.93 ± 0.34 kg N ha-1 a-2, respectively. Consequently, the oceanic and atmospheric changes accounted for 25.7 % ± 28.4 % and 69.0 % ± 42.6 %, respectively, of the Bohai Sea eutrophication mitigation in 2011-2021. On the long-term changes of the Bohai Sea eutrophication, the terrestrial nutrient source has only minor (likely <10 %) impacts, although it certainly affects the spatial distribution of nutrients. This study has implied that coastal eutrophication is a dynamic process that is subject to sea-land-air interactions, and its mitigation needs both local pollution controls and regional environment management. The latter contains the understanding of oceanic changes and external effects of the air pollution control.

Exosomal miR-150 derived from BMSCs inhibits TNF-α-mediated osteoblast apoptosis in osteonecrosis of the femoral head by GREM1/NF-κB signaling.

Aim: The purpose of this study was to investigate the functions of exosomal miR-150 derived from bone marrow mesenchymal stem cells in osteonecrosis of the femoral head (ONFH). Materials & methods: Cell viability and apoptosis were detected using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and flow cytometry. Alizarin red staining was performed to detect calcium deposits. A rat model was established to assess the effects of exosomal miR-150 on ONFH in vivo. Results: Exosomes or exosomal miR-150 derived from bone marrow mesenchymal stem cells inhibited TNF-α-induced osteoblast apoptosis and promoted osteogenic differentiation and autophagy. Exosomal miR-150 suppressed apoptosis and induced autophagy in TNF-α-treated osteoblasts by regulating the GREM1/NF-κB axis. Exosomal miR-150 also improved the pathological features of ONFH in vivo. Conclusion: Exosomal miR-150 alleviates ONFH by mediating the GREM1/NF-κB axis. This study provides a potential therapeutic strategy for ONFH.

Osteonecrosis of the femoral head (ONFH) is an orthopedic disease that frequently occurs in young adults aged less than 50 years. At present, there is no widely accepted curative surgical procedure or drug therapy for this disease. Bone marrow mesenchymal stem cells (BMSCs) play a key role in the progression of ONFH. BMSC-derived exosomes refer to small membrane vesicles that can transfer proteins, miRNAs and mRNAs, which are closely related to the development of ONFH. This study showed that exosomal miRNA-150 derived from BMSCs inhibited TNF-α-induced osteoblast apoptosis and promoted osteogenic differentiation and autophagy by regulating the GREM1/NF-κB axis. In addition, exosomal miRNA-150 alleviated the symptoms of ONFH in rats.

Excess nitrogen in the Bohai and Yellow seas, China: Distribution, trends, and source apportionment.

The Bohai and Yellow seas are marginal seas of the western North Pacific, characterized by coastal eutrophication and populated coastlines. In this work, six survey datasets collected between 2011 and 2018 were used to investigate the excess of dissolved inorganic nitrogen (DIN) related to soluble reactive phosphorus (SRP), referred to as N*, in the Bohai and Yellow seas. High N* of more than 5 µmol kg-1 occurred mostly in the Changjiang and Yellow River plumes and/or near the Jiangsu coast. Away from these river plumes and the Jiangsu coast, however, N* usually ranged from -2.5 to 1.0 µmol kg-1. Combining our field data and previously published data, we found that N* in the Bohai and Yellow seas increased in the 1990s and 2000s, likely caused by the combined effect of atmospheric nitrogen deposition increase and the Kuroshio N* rise. In the 2010s, however, the coastal N* increases stopped. Based on a N*-budgeting approach, marine N (either from in situ decomposition of marine organic matters or from the open seas via current inputs) and non-marine N (either from riverine inputs or from local atmospheric nitrogen deposition) were distinguished. Marine N accounted for 51% ± 38% of DIN in the Bohai Sea and 67% ± 37% of DIN in the Yellow Sea. Although this is a regional study, we suggest that accumulation of atmospheric nitrogen along oceanic circulation pathways dominates the decadal evolution of coastal eutrophication. These findings and new insights may improve management of eutrophication in these two important marginal seas, and will also improve our understanding of nutrient dynamics in other marine systems.

Role of Long Noncoding RNAs ZlMSTRG.11348 and UeMSTRG.02678 in Temperature-Dependent Culm Swelling in Zizania latifolia.

Temperature influences the physiological processes and ecology of both hosts and endophytes; however, it remains unclear how long noncoding RNAs (lncRNAs) modulate the consequences of temperature-dependent changes in host-pathogen interactions. To explore the role of lncRNAs in culm gall formation induced by the smut fungus Ustilago esculenta in Zizania latifolia, we employed RNA sequencing to identify lncRNAs and their potential cis-targets in Z. latifolia and U. esculenta under different temperatures. In Z. latifolia and U. esculenta, we identified 3194 and 173 lncRNAs as well as 126 and four potential target genes for differentially expressed lncRNAs, respectively. Further function and expression analysis revealed that lncRNA ZlMSTRG.11348 regulates amino acid metabolism in Z. latifolia and lncRNA UeMSTRG.02678 regulates amino acid transport in U. esculenta. The plant defence response was also found to be regulated by lncRNAs and suppressed in Z. latifolia infected with U. esculenta grown at 25 °C, which may result from the expression of effector genes in U. esculenta. Moreover, in Z. latifolia infected with U. esculenta, the expression of genes related to phytohormones was altered under different temperatures. Our results demonstrate that lncRNAs are important components of the regulatory networks in plant-microbe-environment interactions, and may play a part in regulating culm swelling in Z. latifolia plants.

[Acupuncture preconditioning at "Zusanli"(ST36) and "Zhongwan"(CV12) prevents stress gastric ulcer by regulating the TLR4/MyD88/IκB signaling pathway].

OBJECTIVE: To observe the effect of electroacupuncture preconditioning at "Zusanli"(ST36，Lower Confluent point) and "Zhongwan"(CV12，Front-Mu point) combination on oxidative stress and inflammation-related indicators, Toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88) and inhibitor-α of nuclear transcription factor κB (IκB-α) in serum and gastric tissue of rats with stress gastric ulcer(SGU)，so as to explore its mechanisms underlying prevention of SGU. METHODS: A total of 36 Wistar rats were randomly divided into blank control, model, positive drug and He-Sea-Front-Mu point combination groups (n=9 in each group). A rat model of SGU was established by restraint water-immersion stress method. Ten days before mode-ling, rats in the He-Sea-Front-Mu point combination group received electroacupuncture （2 Hz, 0.6 mA）at ST36 and CV12 for 10 min once every other day for 10 days, and those in the positive drug group was treated by gavage of omeprazole (20 mg/kg) once every other day for 10 days. The morphology of the gastric mucosa was observed by naked eyes and hematoxylin-eosin staining, and the ulcer index (UI) and lesion score were calculated. TBA and colorimetric methods, ELISA and Western blot were used to detect malondialdehyde (MDA), myeloperoxidase (MPO), glutathione peroxidase (GSH-Px), tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) levels and the relative expressions of TLR4, MyD88, and IκB-α protein, separately. RESULTS: The gastric mucosa of rats in the blank control group was smooth and intact, the cells were arranged neatly, and there was no telangiec-tasia, hyperemia and inflammatory cell infiltration. The gastric mucosal epithelial structure of rats in the model group was destroyed, and a large number of mucosal epithelial cell death and inflammatory cell infiltration were seen. The degree of gastric mucosal injury and inflammatory cell infiltration in the positive drug group and the combined point group was less than that in the model group. Compared with the blank control group, the UI and lesion score of rats in the model group were significantly increased (P<0.05), the levels of MDA and MPO in the serum and gastric tissues were significantly increased (P<0.05), GSH-Px was significantly reduced (P<0.05), the contents of TNF-α and IL-6 in serum were markedly increased (P<0.05), the expression levels of TLR4 and MyD88 proteins in gastric tissue were significantly increased (P<0.05), IκB-α was significantly reduced (P<0.05). After intervention and in comparison with the model group showed that, the UI and lesion score, the levels of MDA and MPO, contents of serum TNF-α and IL-6, expression levels of TLR4 and MyD88 proteins in positive drug and He-Sea-Front-Mu point combination groups were significantly decreased (P<0.05), while GSH-Px and IκB-α were significantly increased (P<0.05); There were no significant differences in the above indicators between the positive drug and the He-Sea-Front -Mu point combination groups （except TNF-α）. CONCLUSION: Electroacupuncture preconditioning at ST36 and CV12 can prevent SGU, which may be related to its effects in anti-oxidant, anti-inflammatory and regulating TLR4/MyD88/IκB signaling pathway.

Improving the understanding of central Bohai Sea eutrophication based on wintertime dissolved inorganic nutrient budgets: Roles of north Yellow Sea water intrusion and atmospheric nitrogen deposition.

The Bohai Sea is a shallow-water, semi-enclosed marginal sea of the Northwest Pacific. Since the late 1990s, it has suffered from nutrient over-enrichment. To better understand the eutrophication characteristics of this important coastal sea, we examined four survey datasets from summer (June 2011), late autumn (November 2011), winter (January 2016), and early spring (April 2018). Nutrient conditions in the Bohai Sea were subject to seasonal and regional variations. Survey-averaged N/P ratios in estuarine and nearshore areas were 20-133. In contrast, the central Bohai Sea had mean N/P ratios of 16.9 ± 3.4 in late autumn, 16.1 ± 3.0 in winter and 13.5 ± 5.8 in early spring, which are close to the traditional N:P Redfield ratio of 16. In summer, both dissolved inorganic nitrogen (DIN) and dissolved inorganic phosphate (DIP) were used up in the surface waters of the central Bohai Sea, suggesting that the biological consumption of DIN and DIP may also follow the Redfield ratio. Wintertime nutrient budgets of the central Bohai Sea water were then established based on a mass balance study. Our results suggest that the adjacent North Yellow Sea supplied additional DIP to the central Bohai Sea via wintertime water intrusion, balancing terrigenous excess DIN that was introduced in summer. A water-mixing simulation combining these two nutrient sources with atmospheric nitrogen deposition suggests that eutrophication in the central Bohai Sea will likely be enhanced by the large-scale accumulation of anthropogenic nitrogen in adjacent open oceans. Such changes in nutrients may have fundamentally contributed to the recent development of algal blooms and seasonal hypoxia in the central Bohai Sea.

TNF-α regulates the early development of avascular necrosis of the femoral head by mediating osteoblast autophagy and apoptosis via the p38 MAPK/NF-κB signaling pathway.

Previous studies have shown that the tumor necrosis factor-α (TNF-α) levels in serum and bone tissues formed in avascular necrosis of femoral head (ANFH) patients were higher than those of normal individuals, indicating TNF-α might play a role in the pathogenesis of ANFH. However, the underlying mechanisms remain unclear. Hematoxylin and eosin staining was performed to show the pathological changes of ANFH bone tissues. TNF-α expression in normal and ANFH tissues was examined by quantitative real-time polymerase chain reaction and western blot analyses. Osteoblast autophagy and apoptosis, as well as signaling pathways activation, were measured by their corresponding marker proteins. Osteoblast proliferation, autophagy, and apoptosis were evaluated using cell counting kit-8, transmission electron microscopy, and flow cytometry. The structures of bone tissues of ANFH were obviously damaged. TNF-α expression was significantly upregulated in ANFH bone tissues compared to normal tissues. Autophagy and apoptosis were remarkably promoted, and p38 mitogen-activated protein kinase (MAPK)/nuclear factor-κB (NF-κB) signaling pathways were markedly activated in ANFH. Suppression of the p38 MAPK/NF-κB pathway significantly attenuated the TNF-α-induced autophagy, however, enhanced the TNF-α-induced apoptosis in osteoblasts. Increased TNF-α in ANFH regulated osteoblast autophagy and apoptosis by p38 MAPK/NF-κB signaling pathways, blocking the pathway by inhibitors exacerbated TNF-α-induced apoptosis through impairing autophagy flux.

Occurrence, sources and health risk of polycyclic aromatic hydrocarbons in soils around oil wells in the border regions between oil fields and suburbs.

The Yellow River Delta (YRD) is a typical region where oil fields generally overlap cities and towns, leading to complex soil contamination from both the oil fields and human activities. To clarify the distribution, speciation, potential sources and health risk of polycyclic aromatic hydrocarbons (PAHs) in soils of border regions between oil fields and suburbs of the YRD, 138 soil samples (0-20 cm) were collected among 12 sampling sites located around oil wells with different extraction histories. The 16 priority control PAHs (16PAHs), as selected by the United States Environmental Protection Agency (USEPA), were extracted via an accelerated solvent extraction and detected by GC-MS. The results showed that soils of the study area were generally polluted by the 16PAHs. Among these pollutions, chrysene and phenanthrene were the dominant components, and 4-ring PAHs were the most abundant. A typical temporal distribution pattern of the 16PAHs was revealed in soils from different sampling sites around oil wells with different exploitation histories. The concentrations of total 16PAHs and high-ring PAHs (HPAHs) both increased with the extraction time of the nearby oil wells. Individual PAH ratios and PCA method revealed that the 16PAHs in soil with newly developed oil wells were mainly from petroleum pollutants, whereas PAHs in soils around oil wells with a long exploitation history were probably from petroleum contamination; combustion of petroleum, fuel, and biomass; and degradation and migration of PAHs from petroleum. Monte Carlo simulation was used to evaluate the health risks of the 7 carcinogenic PAHs and 9 non-carcinogenic PAHs in the study area. The results indicated that ingestion and dermal contact were the predominant pathways of exposure to PAH residues in soils. Both the carcinogenic and non-carcinogenic burden of the 16PAHs in soils of the oil field increased significantly with exploitation time of nearby oil wells.

The Role of IL-27 and its Receptor in the Pathogenesis of HIV/AIDS and Anti-viral Immune Response.

BACKGROUND: Cytokines have been widely demonstrated to involve in the pathogenesis of AIDS and the mechanisms of antiretroviral therapy. Interleukin 27 (IL-27) is a new member of the IL-12 cytokine family and has been shown to interfere HIV-1 virus replication with controversial findings. This study is to investigate the dynamic changes in plasma IL-27 level and cell surface IL-27 receptor expression in HIV/AIDS patients who underwent HAART. METHODS: Whole blood was collected from 34 HIV-positive/AIDS patients 0, 6, and 12 months after initiation of HAART and 27 healthy subjects. Plasma IL-27, IFN-γ, and IL-4 were measured by enzyme-linked immunosorbent assay, while peripheral blood CD3+CD4+ T cells count and the gp130 expressed CD3+CD4+cell were measured by flow cytometry. RESULTS: The plasma IL-27 concentration, IFN-γ concentration, and percentage of positive gp130 CD4 cells were significantly decreased in previously treatment-naive HIV/AIDS patients compared to healthy controls, but gradually increased 6 and 12 months after initiation of HAART. Conversely, IL-4 levels were significantly increased in treatment-naive HIV/AIDS patients compared to healthy controls, but gradually decreased 6 and 12 months after HAART. The concentrations of plasma IL-27 were positively correlated with the percentage of gp130 positive CD4 cells (r=0.438, p=0.016). Both plasma IL-27 concentration and gp130 positive cell percentage were positively associated with peripheral blood CD3+CD4+ T cell count (P<0.05 or P<0.01), but negatively associated with plasma HIV viral load (P<0.05 or P<0.01). CONCLUSION: IL-27 signaling (IL-27 and its receptor) may be involved in the pathogenesis of HIV infection and immune reconstitution in HIV/AIDS patients who underwent HAART. IL-27 may exert effects through regulating Th1 / Th2 ratio.

[Detection of Carbon Dioxide Concentration in Soil Profile Based on Nondispersive Infrared Spectroscopy Technique].

In order to explore the variation of CO2 concentration and soil respiration in soil profile, the nondispersive infrared (NDIR) spectroscopy technique was applied to continually estimate the soil CO2 concentration in different soil layers (the humus horizon, A-, B-, C-horizon) in situ. The main instrument used in this experiment was silicon-based nondispersive infrared sensor, which could work in severe environment. We collected the Measurement value by NDIR spectroscopy technique throughout 2013. The values of soil carbon flux in different soil layers were calculated based on the model of gradient method and calibrated by measuring with an automated soil CO2 efflux system (LI-8100). The results showed that: a vertical gradient for the carbon dioxide concentration in soil profile was found, and the concentration was highest in the deepest soil horizon. Moreover, A linear correlation between the soil CO2 effluxes was calculated based on model and measurement, and the model prediction correlation coefficient was 0.9069, 0.7185, 0.8382, and 0.9030 in the H-, A-, B-, and C-horizon, respectively. The roots of mean square error (RMSE) were 0.2067, 0.1041, 0.0156, and 0.0096 in the H-, A-, B-, and C-horizon, respectively. These results suggest that the gradient method based on the NDIR spectroscopy technique can be successfully used to measure soil CO2 efflux in different soil layers, which reveal that diffusion and convection transport CO2 between the soil layers. It is a promising sensor for detecting CO2 concentration in soil profile, providing the basic data for calculating the global carbon in soil profile.

[Influence of chronic intermittent hypoxia on sympathetic nerve activity in rats and effect of the antioxidant Tempol].

OBJECTIVE: To study the role of sympathetic nerve activity during the development of hypertension resulting from chronic intermittent hypoxia, and whether or not elevated sympathetic nerve activity is related to oxidative stress, and to investigate the preventive effect and possible mechanism of Tempol. METHODS: Forty-eight male Wistar rats were randomly divided into 6 groups of 8 each, including normoxic control group (NC), intermittent hypoxia group (IH) and 4 treatment groups (IHT1, IHT2, IHN1, IHN2). Among the treatment groups, IHT1, IHT2 groups were treated with 10% Tempol 100 mg × kg(-1)× d(-1) by intraperitoneal injection before exposed to IH and on day 28 after exposed to IH respectively, while IHN1 and IHN2 groups were treated with NS as controls. RESULT: There was no statistic difference in artery systolic blood pressure (SBP) between IH group, IHN1 group [(114 ± 6) mm Hg, 1 mm Hg = 0.133 kPa], and IHN2 group [(128 ± 6) mm Hg, P < 0.05] at the end of 6(th) week. SBP in the all IH groups was significantly elevated compared with NC group (P < 0.05) and the baseline SBP (P < 0.05) except of the group IHT1. SBP in the 2 tempol treatment groups was lower than the NS groups [(138 ± 10) mm Hg, both P < 0.05], while SBP of IHT2 group was higher than the IHT1 group (P < 0.01). No significant changes were found in the NC group. There were no statistic difference of NE and E in plasma and MDA in adrenal gland tissues between IH groups, IHN1 group and IHN2 group. The levels in NE and E and MDA in the 2 tempol treatment groups were lower than the NS groups (P < 0.05 or P < 0.01), but those in the IHT2 group were higher than the NC group (P < 0.05 or P < 0.01) and IHT1 groups (P < 0.05 or P < 0.01). No significant difference were found between IHT1 group and NC group. CONCLUSION: CIH could generate ROS by causing oxidative stress, which results in elevated sympathetic nerve activity. This may be one of the important mechanisms for CIH-induced hypertension. Tempol may be useful for prevention and treatment of OSAS-induced hypertension.

[Hepatic injury in rats exposed to chronic intermittent hypoxia and the effect of tempol].

OBJECTIVE: To investigate the mechanism of liver injury in rats exposed to chronic intermittent hypoxia (CIH) and to investigate the effect of tempol (4-hydroxy-2,2,6,6-tetramethylpiperidine-N-oxyl or 4-hydroxy-TEMPO). METHODS: A CIH animal model of rats was established to mimic the intermittent hypoxia/re-oxygenation (IH/ROX) of obstructive sleep apnea syndrome in humans. Thirty-two healthy male Wistar rats were randomly assigned to 4 groups: conventional intermittent hypoxia group (CIH group), intermittent hypoxia Tempol treatment group (CIH + T group), intermittent hypoxia normal saline matched group (CIH + NS group), and normoxic control group (NC group), with 8 rats in each group. The frequency of every CIH group was 30 times/h, and the minimum oxygen concentration was 5%. After the experiment, sections of liver were stained with hematoxylin-eosin (HE) and the levels of nuclear factor-kappaB (NF-κB), glutathione peroxidase (GSH-PX) and malondialdehyde (MDA) in rat liver homogenate were measured. RESULTS: Liver histology revealed that the CIH group and the CIH + NS group showed hepatocellular swelling with rarefaction of the cytoplasm, hyperchromatosis and hepatocellular membrane disruption, but the liver histology of the CIH + T group and the NC group was normal. Compared with the NC group, the levels of NF-κB and MDA in the CIH group [(12.4 ± 2.0) ng/g, (101 ± 22) µmol/g] and the CIH + NS group [(12.2 ± 1.9) ng/g, (99 ± 18)µmol/g] were increased (all P < 0.05), but the activities of GSH-PX [(88 ± 17) U/mg, (90 ± 15) U/mg] were decreased (all P < 0.05). Compared with the CIH + NS group and the CIH group, the activity of GSH-PX in the CIH + T group [(181 ± 29) U/mg] was increased (P < 0.05), but the levels of NF-κB [(7.8 ± 1.3) ng/g] and MDA [(59 ± 10) µmol/g] were decreased (all P < 0.05). The levels of GSH-PX and MDA in the CIH + T group were not significantly different compared to the NC group (P were 0.242, 0.177 respectively), but the level of NF-κB in the CIH + T group was higher than that in the NC group (P < 0.05). The levels of NF-κB, GSH-PX, and MDA in the CIH + NS group were not significantly different as compared to those in the CIH group (all P > 0.05). The level of NF-κB was correlated negatively with GSH-PX, but positively with MDA (r = -0.754, 0.689, respectively, all P < 0.01) CONCLUSIONS: CIH could cause rat liver injury through oxidative stress and activating the proinflammatory transcription factors of NF-κB. Tempol could prevent CIH-induced liver injury through scavenging ROS by its anti-oxidative effect.

[Clinical characteristics of highly active antiretroviral therapy-associated immune reconstruction inflammation in acquired immunodeficiency syndrome].

OBJECTIVE: To summarize the morbidity, mortality, clinical manifestations and risk factors for IRIS (immune reconstruction inflammatory syndrome) during HAART (highly active antiretroviral therapy) in China. METHODS: From October 2007 to September 2009, a prospective cohort of 238 AIDS (acquired immunodeficiency syndrome) patients on HAART from Hunan and Jianxi provinces was recruited for a follow-up of 24 weeks. And 47 and 191 patients were assigned into the IRIS and non-IRIS groups respectively. The data of general information, clinical manifestations and treatment of two groups were collected and compared. Blood samples were collected in both groups at pre-and post-HAART 12 weeks, 24 weeks for HIV viral load and CD4(+) cell count examinations. A statistical analysis was performed. RESULTS: A total of 47 (19.7%) IRIS cases was analyzed. The median onset of IRIS was 28 (9 - 36) days. And 29 (61.7%) cases of tuberculosis IRIS were found. There was no significant difference in age, gender, route of transmission and antiretroviral regimens between the IRIS and non-IRIS groups. At baseline, Weeks 12 and 24, both groups showed a significant decline of viral load. And there was no significant difference between them. Both groups showed a significant increase of CD4(+) cell count. But there was no significant difference between two groups. However, the baseline CD4(+) cell count was markedly lower in the IRIS group than that in the non-IRIS group. In 85.1% (40/47) of cases, the CD4(+) cell count was < 100 × 10(6)/L in the IRIS group at the baseline of HAART. CONCLUSION: IRIS mostly occurs during 3 months of HAART initiation. The age, gender, route of transmission and antiretroviral treatment regimens of patients on HAART are not risk factors for the development of IRIS. The HIV RNA viral load decreases in both IRIS and non-IRIS groups without any significant difference. The patients with a CD4(+) cell count < 100/µl are more vulnerable to develop IRIS.