, 2005). At Xiaodeshi in the Yalong River, a tributary of YTR, the GDC-0941 molecular weight June–October discharge is 77% of the annual total (Chen et al., 2012). Rainfall contributes the most to the annual total streamflow at Zhimenda, Shigu and Xiaodeshi (Table 2). Annual flow showed slightly increasing trends at Zhimenda during 1961–2011 (Li et al., 2012a and Li et al., 2012b), at Xiaodeshi during 1956–2004 (Cao et al., 2005 and Chen et al., 2012),

and at Shigu in the lower reach during 1953–2005 (Xu et al., 2010 and Zhao and Gao, 2011) (Table 3). The negative trends in annual total are noted at Yushu during 1956-2000 (Table 3) and the reason is unknown (Zhou et al., 2005). The Tuotuo River, the headwater of YTR and located above Yushu, exhibited an increasing trend in streamflow during

the late 1950s–2000 (Table 3; Yang et al., 2003, Jin et al., 2005, Zhang et al., 2008, Liu et al., 2009 and Bing et al., 2011), indicating that the main contributor to the Tuotuo River is melt water that is enhanced by increasing temperature. The difference in streamflow change between Tuotuo River and Yushu implies that as the basin expands to the lower elevation, melt water contribution diminishes and the other influence becomes more important. In MKR, the June–September discharge accounts for 70% of the annual total at Changdu, with combined melt water and groundwater contributing much more than rainfall (Table 2; Wang, 2007 and Lu et al., 2009). Streamflow change at Xiangda during 1956–2000 showed decreasing trends before 1980 but increasing trends after 1980, though the trends GSK458 clinical trial were not statistically significant (Table HAS1 3; Zhou et al., 2005). Also, the date of the mid-point of yearly flow shifted earlier at Xiangda during recent decades (Xu et al., 2004 and Lu et al., 2009). At Changdu that is located below Xiangda, Cao et al. (2005) found statistically insignificant increasing trends in streamflow during 1968–2000 (Table 3); on the other hand, Zhang et al., 2012a and Zhang et al., 2012b showed that during 1958–2005 streamflow at Changdu exhibited statistically

insignificant decreasing trends in annual, flood and non-flood seasonal flows. The differences between Cao et al. (2005) and Zhang et al., 2012a and Zhang et al., 2012b are due to the different datasets, methods and study periods used. It is possible that Cao et al. (2005) only showed a partial change of streamflow over a longer period 1958–2005. For IDR, Senge Zangbu and Langqin Zangbu are the headwaters that are fed primarily by groundwater and melt water (Table 2). In Senge Zangbu groundwater and melt water together account for about 84% of the annual streamflow, with 55% of the annual flow occurring in July–September (Guan and Chen, 1980). Due to lack of reports on IDR within China, streamflow change is virtually unknown. In BPR, the June–September flow accounts for 65–75% of the annual total at stations located along the main branch (Liu, 1999).

In addition, Corner et al. (22) reported on a Phase II trial from the United Kingdom that includes 110 men with locally advanced

disease treated with HDR monotherapy to doses of 34 Gy in four fractions, 36 Gy in four fractions, or 31.5 Gy in three fractions. The rate of acute urinary retention requiring catheterization was 6.4%, and there Obeticholic Acid molecular weight were no PSA relapses with a median followup of 30 months (34 Gy), 18 months (36 Gy), and 11.8 months (31.5 Gy). Also, Yoshioka et al. (23) has reported on a Japanese series of 112 men treated with hormonal therapy and HDR monotherapy to 54 Gy in nine fractions over 5 days in which the 5-year PSA failure-free survival was 83%despite more than one-half of the patients having high-risk disease. Finally, Mark et al. (24) of Lubbock, Texas have presented

in abstract form on their large series of 312 HDR monotherapy patients treated to 4500 cGy in six fractions to the prostate and seminal vesicles given as two implants of three fractions each, spaced 4 weeks apart. None of the patients received ADT, and with a median followup of 8.2 years, the PSA failure-free survival was 84.6%. In the setting of prior pelvic radiation, UCSF investigators have published two series using a regimen of 36 Gy in six fractions given as three fractions per implants, with the implants being spaced 1 week apart. The first series by Lee et al. (1) in 2007 detailed 21 patients who had received prior external beam radiation (19) or LDR brachytherapy (2) for prostate cancer and developed a biopsy-proven local recurrence at an average of 5.25 years after initial radiation. IDH inhibition Nine of the patients had extracapsular extension or seminal vesicle invasion. Eleven received neoadjuvant ADT before salvage HDR. The 2-year PSA failure-free survival was 89% and the maximum gastrointestinal toxicity was only Grade 2, but the median followup was only 18.7 months.

The second series by Jabbari et al. (2) was of 6 patients who developed prostate cancer after receiving a prior abdominopelvic resection. All had received prior pelvic radiotherapy to a median dose of 45 Gy (range, 21–73.8 Gy). FER With a median followup of 26 months (range, 14–60months), no patient had experienced a biochemical recurrence, and none had higher than a Grade 3 acute toxicity, although 1 patient developed a urethral stricture that required dilation. Rectal fistula is a very rare complication of primary brachytherapy in patients who have not received prior radiation (25). However, it has been reported in 3.4% of the 251 cases of salvage brachytherapy reported in the literature from 1990 to 2007. The Dana–Farber Phase I/II study identified an interval to reirradiation of less than 4.5 years as a risk factor for developing a fistula, which placed our patient at higher risk because his interval to reirradiation was only 2.5 years. However, no dosimetric risk factors for fistula have been identified in this setting, and therefore the goal was to keep the rectal dose as low as possible.

1. Atlantic surface water flows into the Mediterranean Sea through the upper layer of the Gibraltar Strait and mixes with WMB surface selleck water. Part of the surface WMB water then flows through the upper layer of the Sicily Channel to the EMB and mixes with EMB surface water. Net precipitation and river discharge influence the

water and heat balances in both sub-basins as well as the exchange with the Black Sea. In the winter, convection occurs because of the negative water balance in certain areas of the northern EMB, forming the deep-water outflow through the Sicily Channel to the WMB (Zervakis et al., 2000). This lower flow together with deep-water formation in the Gulf of Lion (in the northern WMB) is responsible for the dense water outflow through the Gibraltar Strait to the Atlantic Ocean. The Mediterranean Sea’s large-scale inverse estuarine circulation is driven

by the water balance, causing dense bottom-water formation due to strong evaporation and outflowing dense water through the Sicily Channel and Gibraltar Strait into the Atlantic Ocean, with compensating for Atlantic Ocean surface water flowing into the Mediterranean Sea. The present version of the model uses the PROBE equation solver for the Mediterranean Sea called PROBE-MED Selleckchem Stem Cell Compound Library version 2.0. PROBE-MED version 2.0 focuses on such processes as diapycnal mixing, inverse estuarine circulation, and land–air–sea interactions in the Mediterranean Sea. The exchange through the Strait of Messina Masitinib (AB1010) and Suez Canal are neglected as they are smaller than the exchange through the Sicily Channel and Gibraltar Strait. The Black Sea is treated as a river flow into the EMB, as in the earlier study (Shaltout

and Omstedt, 2012). Consequently in- and outflows are addressed by the exchange through the Gibraltar Strait and Sicily Channel. The Black Sea together with, in order of declining importance, the Nile, Po, Ceyhan, Adige, Drin, Vjose, Marista, Buyuk Menderes, and Shkumbini rivers are considered the dominant sources of fresh water to the EMB with a combined annual mean discharge of 11,209 m3 s−1. The decreasing freshwater flows from the Black Sea and the River Nile play a significant role in the increasing salinity of the EMB: Black Sea discharge decreased by 9.8 × 10 m3 s−1 yr−1 from 1958 to 2009 due to decreasing net precipitation (Shaltout and Omstedt, 2012 and Stanev and Peneva, 2002), while the Nile River discharge was reduced by a factor of more than two after the Aswan high dam was built in 1964 (Ludwig et al., 2009). The Rhone, Ebro, Tiber, Jucar, Cheliff, Moulouya, Mejerdah, and Tafna rivers are considered the dominant sources of fresh water to the WMB with an annual mean discharge of 2811 m3 s−1. Mediterranean Sea deep water forms in the winter because of evaporation and heat losses. The Adriatic, Aegean, and Levantine sub-basins are the significant sources of EMB deep water (Malanotte-Rizzoli et al., 1999).

, 2000 and Vogt et al., 1998) whereas during actual task performance, small power (large event related desynchronization or ERD) is related to good performance (e.g., Doppelmayr et al., 2005 and Klimesch et al., 1997). Most interestingly for perceptual performance (in tasks target detection under threshold or near threshold conditions), small prestimulus alpha power (Ergenoglu et al., 2004) and a small ERD or even event related synchronization (ERS) during actual task performance (Hanslmayr et al., 2005) is predictive for good performance. A variety of studies have meanwhile documented

that a state CAL-101 in vitro of low prestimulus alpha power is associated with improved detection and discriminability of threshold-level stimuli (Hanslmayr et al., 2007a, Mathewson et al., 2009, Romei et al., 2007, Romei et al., 2008 and Van Dijk et al., 2008). There is, thus, good evidence for a double dissociation between pre- and poststimulus alpha power and the type of cognitive

PLX4032 in vitro performance. Good memory performance is associated with large prestimulus but small poststimulus alpha power, whereas good perception performance is related to small prestimulus power with little or no ERD during perception performance. We have interpreted these findings in terms of cortical inhibition and excitation preceding task performance. Perception performance appears to be enhanced if the cortex already is activated (as indicated by small prestimulus power), whereas memory performance is enhanced if the cortex is

not activated (as indicated by large prestimulus power) before a task is performed. This interpretation is quite plausible if we assume Wilson disease protein that for visual target detection a high level of cortical excitation will be helpful to analyze a visual input. When a specified and well known target must be detected, memory traces are probably ‘preactivated’ and as a consequence inhibition must be reduced. For memory performance, on the other hand, an initial (prestimulus) activation of the cortex may be detrimental because it may interfere with (or even suppress) the high selectivity that is required for accessing a memory trace during actual task performance. In considering these findings and their interpretation, let us now make predictions for a traditional spatial cuing task in which a target must be detected in the right or left visual field. The prediction for prestimulus alpha power at the contralateral side is a decrease in power, whereas for the ipsilateral side, we expect an increase in power. Because the functional meaning of the P1 amplitude is similar to that of ongoing alpha, we also expect a larger ipsilateral P1. We have tested this prediction in Experiment 1 of the study by Freunberger et al. (2008a). As observed in other studies (e.g., Busch et al. 2004), we also found that the P1 is larger over ipsi- as compared to contralateral recording sites. In our study (using a type 2 paradigm with a jittered ISI between cue and target; cf. Freunberger et al.

Ultimately, by understanding fundamental aspects of RNA modification biology we will be able to develop selective and specific small-molecule selleck chemicals llc inhibitors to modulate RNA methylation levels. Such discoveries may well lead to the identification of novel

therapeutic strategies to treat complex diseases including developmental and neurological disorders, obesity or cancer. Papers of particular interest, published within the period of review, have been highlighted as: • of special interest We gratefully acknowledge the support of the Cambridge Stem Cell Initiative and Stephen Evans-Freke. We thank our funders Cancer Research UK (CR-UK)

(C10701/A15181), the Medical Research Council (MRC) (G0801904), the European Research Council (ERC) (310360), and EMBO (Grant no. ALTF 424-2008). “
“Current Opinion in Cell Biology 2014, 31:16–22 This review comes from a themed issue on Cell cycle, differentiation and disease Edited by Stefano Piccolo and Eduard Batlle For a complete overview see the Issue and the Editorial Available online 12th July 2014 http://dx.doi.org/10.1016/j.ceb.2014.06.011 0955-0674/© 2014 The Authors. Published by Elsevier Ltd. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/3.0/). TSA HDAC Darwin’s theory of natural selection has revolutionized our understanding of how organisms evolve. Often, the essence of his theory is formulated with ‘the fittest survive’, a term first coined by Herbert Spencer, to summarize the ideas of Darwin Clomifene that better adapted organisms will live to have more offspring. In 1881, zoologist

Wilhelm Roux argued that Darwinian competition and selection had not been considered for the development of tissues and organs. In his view, cells within our bodies were also likely to compete for space and limited resources. Such ‘fights’ among slightly varying ‘parts of our bodies’ would result in the ‘selective breeding’ of the most durable and the elimination of less durable parts (cells). Along similar lines, Santiago Ramon y Cajal proposed a few years later that developing neurons may be engaged in a competitive struggle for space and nutrition, an idea which gained support in the framework of the neurotrophic theory and the discovery of nerve growth factor by Rita-Levi Montalcini and its isolation by Stanley Cohen in 1960 [1]. During nervous system development, large proportions of neurons die in almost every region of the nervous system. The normal death of these neurons occurs during a limited time window coinciding with target innervation [2].

Canaud et al. (2005) investigated the pharmacological toxicity of PF-5070 in rabbits [9]. Rabbits were given the low (4 μL/kg) or intermediate dose (40 μL/kg) exhibited generalized malacia of the cerebrum and cerebellum. Notably, one animal showed

horizontal nystagmus and pulmonary infarcts were detected in some rabbits given the intermediate dose. Neurologically MLN0128 mouse positive animal in the intermediate and high dose (160 μL/kg) groups showed hemorrhagic or ischemic damage in the cerebrum and cerebellum. The necrosis was sharply demarcated from adjacent viable tissue, a characteristic morphologic sign of ischemic infarct. Histopathologic findings from other organs in their study were extensive pulmonary edema, hemorrhages and infarction, and disseminated patchy necrosis of kidney, liver and spleen. In our study, SpO2 was screening assay remarkably decreased in both the PL and AA groups without histological damage. There was no macrophage phagocytosis of MBs or necrosis in the lungs, liver, spleen or kidneys. These phenomena may have been due to transient pulmonary alveolar occlusion while intravascular SPNs were present before they were excreted to the air. This speculation

could be extended to the animal with transient nystagmus in the AA group without cerebellum and brain stem damage. According to the study by Canaud et al. and our study, i.v. administration of PFC in rabbits might have the potential to cause occlusion within the vertebrobasilar system [9]. Moreover, one animal in the PL group Vorinostat clinical trial that died after injection did not appear to have leukocyte aggregation or macrophage hypertrophy in the lungs [12]. However, the causes may also be attributable to delayed allergic reaction or some other unknown factor related to SPN injection. In summary, the

side effects of our newly developed SPNs are reversible respiratory disturbance and transient horizontal nystagmus without permanent neurological deficits, and biochemical changes in the plasma. One animal in the PL group died apparently of delayed shock. The most noteworthy point in this study is that no pathological damage due to gas embolism was found in any organs, including the brain tissue of case that developed temporary nystagmus. Our next challenges for novel neurological US therapies including sonothrombolysis are further evaluation of the safety administration dosages, other kinds of SPNs, and research into transcranial US trigger conditions which can convert SPNs into MBs in the cerebrovascular system. No permanent neurological deficit, biochemical changes in plasma, or histological damage were observed after injection of the two SPNs in surviving animals. One animal in the PL group died of delayed shock 2 days after injection. This study was supported, in part, by the New Energy and Industrial Technology Development Organization, Japan.

36 (line d), and 19.22 ± 0.42 (line e); differences statistically significant were found between (line a) and the other lines, at P < 0.05. Both NAD(P)H depletion/oxidation ( Fig. 9A) and ROS levels increase ( Fig. 9B) by GA (lines b) were partially prevented by the replacement of NADPH by isocitrate (lines c). These results suggest that GA-induced mitochondrial membrane potential dissipation renders transhydrogenase unable to sustain the reduced state of NADPH and allows mitochondria to accumulate ROS. A decrease in fluorescence anisotropy (r) reflects increase in DPH mobility into membranes and decrease in membrane structural order/increase of membrane fluidity. Fig. 10 shows that GA interacts

with mitochondrial membrane increasing its fluidity. The effects of GA in the present study were compared with the check details effects of the classic mitochondrial uncoupler CCCP since GA displayed uncoupling action both in HepG2 Pexidartinib clinical trial cells and rat liver isolated mitochondria. It is worthy to consider that most of these effects have been frequently associated with mitochondria-mediated cell death (Kroemer et al., 1995, Skulachev, 2006 and Xia

et al., 2009). Indeed, GA and other structurally related compounds present several proposed biological actions (Gustafson et al., 1992, Ngouela et al., 2006, Pereira et al., 2010 and Williams et al., 2003), including well-documented toxicity toward cancer cells (Baggett et al., 2005, Cao et al., 2007, Huang et

al., 2009, Matsumoto et al., 2003, Merza et al., 2006, Pan et al., 2001, Sang et al., 2001, MRIP Williams et al., 2003 and Xu et al., 2010). In addition to these previously proposed actions, we here provided for the first time evidence that GA may interact with mitochondrial membrane and presents both energetic and oxidative stress implications: a cyclosporine A/EGTA-insensitive mitochondrial membrane permeabilization, mitochondrial uncoupling (membrane potential dissipation/state 4 respiration rate increase), Ca2+ efflux, ATP depletion, mitochondrial NAD(P)H depletion/oxidation and ROS levels increase. NAD(P)H depletion/oxidation probably resulted from the mitochondrial membrane potential dissipation, a condition in which the NADP+ transhydrogenase is unable to sustain the reduced state of mitochondrial matrix NADPH. NADP+ transhydrogenase is a mitochondrial membrane enzyme responsible for driving the reduction of NADP+ by NADH coupled to the proton motive force (chemical and electrical potential energy) (Hatefi and Yamaguchi, 1996 and Hoek and Rydstrom, 1988). NADPH, in turn, is implicated in cell antioxidant defenses involving glutathione (GSH) and thioredoxin (TRX), either reductants themselves or cofactor for GSH and TRX peroxidases; GSH and TRX reduced species are regenerated by NADPH-requiring reductases (Carmel-Harel and Storz, 2000). Therefore, whether NADPH is oxidized/depleted, ROS tend to accumulate.

The authors also would like to thank professor Sandra Regina Paulon Avancini for her assistance in obtaining the necessary resources, masters Márcio Zílio and Aureanna Negrão for their help to perform the analysis and the Santa Catarina State University for giving space and equipment to perform the research. “
“The definition Panobinostat research buy of quality is very complex within the food industry. In the literature

it is very common to find a mixture of quality, the concept, with quality, the measurement or attribute (Bremner, 2002, chap. 10). Botta (1995) defined some main quality attributes with respect to seafood: safety, nutritional characteristics, availability, convenience, integrity and freshness. The most important methods to evaluate freshness of seafood are the sensory methods (Bonilla, Sveinsdóttir, & Martinsdóttir, 2007). Freshness loss of seafood is the result of postmortem biochemical, physicochemical and microbiological processes characteristic of each species and influenced by handling on board and on land and by technological processing (Huidobro, Pastor, & Tejada, 2000). These changes are perceived and can be evaluated in sensory

terms by sight, touch, smell and taste (Huidobro et al., 2000). The Quality Index Method (QIM), originally Dasatinib developed by the Tasmanian Food Research Unit (TFRU), is a descriptive, fast and simple method to evaluate the freshness of seafood (Huidobro et al., 2000). This seafood freshness grading system (Sveinsdóttir, Martinsdóttir,

Jorgensen & Kristbergsson, 2002) is based on significant sensory parameters Ibrutinib supplier for raw fish and a score system from 0 to 3 demerit points (Barbosa and Vaz-Pires, 2004, Branch and Vail, 1985, Bremner, 1985 and Larsen et al., 1992). It evaluates sensory parameters and attributes that change most significantly, in each species, during degradation processes (Huidobro et al., 2000). Therefore higher scores are given as storage time progresses. Each fish species has its own characteristic spoilage patterns and indicators, and consequently QIM schemes must be species-specific (Hyldig and Green-Petersen, 2004, Nielsen and Green, 2007 and Sveinsdóttir et al., 2002). Barbosa and Vaz-Pires (2004) compiled a list of the QIM schemes available. At the time, 21 different fish species or products had specifically designed QIM schemes, while between 2002 and 2009 additional QIM schemes were built for 16 new seafood items. Table 1 summarises the schemes that were created and made available in the scientific literature within that period. In the second period (2002–2009), some of the schemes proposed for the first 21 species were repeated and/or corrected; these recent advances and new schemes can be found on the site of the international project QIM-EUROFISH (www.qim-eurofish.com).

Cellular stress, in addition to cellular necrosis, may thus turn out to be an important mechanism for IL-33 release in vivo. Proteases have been shown to regulate IL-33 activity (Figure 2). IL-33 contains a consensus site of cleavage for caspase-3 (DGVD178G in human), and cleavage by caspases at this site generates two biologically inactive products [45 and 46]. Inactivation of IL-33 during apoptosis is likely to be important to avoid alerting the immune system unnecessarily

after physiological programmed (apoptotic) cell death, as opposed to pathological (necrotic) cell death [45 and 46]. By contrast to caspases which inactivate IL-33, proteases released during inflammation appear to increase IL-33 biological Bafilomycin A1 order activity [49••]. Neutrophil serine proteases, cathepsin G and elastase, were found to process full length IL-33 into mature forms containing the IL-1-like cytokine domain (IL-3395–270, IL-3399–270 and IL-33109–270), that had greatly increased biological selleckchem activity (∼10 fold) compared to the full length protein [49••]. Both full length and mature endogenous IL-33 were detected in BAL fluids in a model of acute lung injury associated with high levels of neutrophil recruitment in the alveolar wall [49••]. Together, these results suggested that proteolytic processing of IL-33 may be required for the extracellular generation of highly active cytokine in vivo.

IL-33 is an alarmin cytokine from the IL-1 family, which plays a crucial role in the initiation of type-2 immune responses following infection with parasites or viruses, or exposure to allergens. IL-33 appears to act by activating ILC2s for production of large amounts of type-2 cytokines IL-5 and IL-13. The potent activity of IL-33 on ILC2s and

the crucial role of these cells in the initiation of allergic airway inflammation are likely to explain the dominant role of the IL-33/ST2 pathway in genetic susceptibility to human asthma. Despite these important advances, many questions remain to be answered. For instance, the potential Tolmetin redundancy or synergy of IL-33 with other activators of ILC2s, that have been recently identified (Prostaglandin D2, Leukotriene D4, IL-9, etc.), needs to be studied. Although the functions of IL-33 in the activation of ILC2s and the initiation of allergic inflammation in the lungs have been well established, its roles in allergic and non-allergic inflammation in other tissues, exhibiting high expression levels of the endogenous protein, remain to be fully explored. A better understanding of IL-33 release, mode of action and regulation will be crucial for the development of therapeutics that target the IL-33/ST2 pathway to treat asthma and other inflammatory diseases. Papers of particular interest, published within the period of review, have been highlighted as: • of special interest We thank members of the Girard lab for fruitful discussions.

Hence coupling both the pretreatment and subsequent enzymatic hydrolysis process would enhance the sugar yields. Cellulose metabolization by the enzymatic activities of JS-C42 on different substrates were given in Fig. 2a–c. The cellulolytic microbial inoculum was grown on medium with cellulose and degradation of cellulose initiated immediately

by the metabolic enzymes secreted by them. Beyond the lag phase after 6 h incubation, the polymeric cellulosic substrate (Cellulose, HiMedia) was consumed at a faster rate, indicating an exceptionally high rate of degradation of cellulose by the isolate JS-C42 and it had been highly efficient when compared to the cellulolytic activities of T. reesei. However the breakdown pattern of Sigmacell was slow when compared to the HiMedia cellulose. NU7441 concentration The cellulolytic isolate JS-C42 achieved the maximum cellulolytic action between check details the periods of 54–78 h of incubation. The maximum sugar content released from HiMedia cellulose and Sigmacell cellulose by JS-C42 was observed at

66 h of incubation with 287 ± 9 and 152 ± 8 μg mL−1 reducing sugar content respectively ( Fig. 2a). Culture supernatants of cellulolytic bacterial isolate JS-C42 were analyzed for reducing sugars, which began to accumulate during the growth on different agricultural biomass; paddy straw, paddy straw with glucose, dry and green sorghum stubbles with the high level of enzymatic saccharification between the periods of 54–78 h Fenbendazole after inoculation. The maximum enzymatic breakdown of lignocellulosic biomass by JS-C42 and the level of reducing sugar concentrations were observed as 198 ± 9 to 202 ± 8, 154 ± 8 to 156 ± 7 and 183 ± 6 to 193 ± 3 μg mL−1 at 60–66 h from paddy straw, dry and green sorghum stubbles respectively. At the end of experimental reactions, the reducing sugars detected as 122 ± 5, 45 ± 7 and 101 ± 4 μg per mL (Fig. 2b), however the quantity was less when compared at 60–66 h of inoculation. The biologically active cellulase enzyme

complex has been produced by JS-C42 in order to utilize the biomasses of tree crops. In case of A. mangium pods and leaves, the steam pretreatment released certain level of reducing sugars (97 ± 4 to 104 ± 4 μg mL−1 and 63 ± 3 μg mL−1 respectively from leaf and pod extract) and all those sugars were utilized by the cellulolytic bacterial isolate JS-C42 within 12 h incubation at 30 °C. Beyond this time, again the reducing sugars started to accumulate in the medium due to the lignocellulolytic action and the maximum sugar content was released during the period of 48–78 h ( Fig. 2c). The sugar release pattern was higher when compared to the cellulolytic effect exerted by the T. reesei. The sugar content released by T. reesei from A. mangium leaf was observed maximum at 48 h onwards and maintained almost at a constant level for a period of 168 h. In case of F.